Home Posts tagged "Weight Loss" (Page 2)

21st Century Nutrition: An Interview with Precision Nutrition Creator, Dr. John Berardi

Normally, my newsletters are "hidden" pages available only to our subscribers, but with the content today, I thought I'd open it up to the rest of the world.  After all, it's not like you can just get a rock star like Dr. John Berardi to do an interview for your site.  JB has been a friend and incredible resource to me for almost ten years now, and he's always got great information to share.  So, without further ado, here is EricCressey.com's exclusive interview with Dr. John Berardi: EC: First off, it's hard to believe that over the course of almost 150 newsletters, I never got around to interviewing you.  Thanks for taking the time to jump in on this. JB: Yea, tell me about it.  I've been waiting by the phone for, like, three years now. EC: Well, now that you've gone through all that therapy to get over me neglecting you, we might as well right to it.  To start, fill us in on what you're up to these days.  I know you moved back from Texas to the North Pole a while back, but I'm guessing that you aren't building toys and stuffing stockings all year.  What's new with John Berardi and Precision Nutrition? JB:  Well, although working with high-level athletes is cool and all, when Santa calls for nutrition advice, you drop what you're doing and you head north. In all seriousness, though, I'm actually splitting my time between Austin, Texas and a town called St. Catharines in Ontario.  St Catharines is about 50 min outside Toronto and is basically the Napa Valley of Canada.  The area is a tremendous agricultural gem and because of this, I have a never-ending supply of locally grown produce and wines as well as local, hormone-free, and often grass fed meat.  So now, I've got two great towns to call my home. EC: I hear you.  When I was considering the move to Boston, the lack of grass-fed beef and local wines was a bit of a turnoff, but it was a sacrifice that I was willing to make because I just couldn't wait to sink my life savings into the Big Dig and the most inefficient state government in the United States - but I digress... How about the professional side of things? JB: On the professional side, I just did a tally.  As of last week, the Precision Nutrition community has grown to over 46,000 members in over 97 countries.  I can't tell you how proud I am that we've been able to help out that many people. And beyond this, we've also launched a couple of new programs for members of the community - our Lean Eating Coaching Program and our Clinical Services Program. EC: 97 countries?  Don't you want to just give out a few freebies in a few lesser known African nations to bring it to a cool 100?  I would. Anyway, tell us about these two new things. JB: First, our Lean Eating coaching program.  Over the last few years, we've become coaching experts, working with everyone from recreational exercisers, to folks suffering from cardiovascular disease and diabetes, to multiple Olympic medalists. And as a result of this experience, we've developed intensive group coaching programs for men and for women.  Each coaching participant gets to work with us for 6 months.  And the feedback we've gotten is tremendous - and so are the numbers.  The average fat loss is 2-3lbs per month while following the program! In addition, we're in the process of launching a clinical services suite where we're taking individualization to a whole new level.  Using things like psychometric profiles, wellness-based blood analysis, and nutrigenomics profiling, we're now able to take a peek inside people's psychologies and physiologies to determine the absolute best way to coach them to success.  This is like nothing our industry has seen before and I promise it's going to shake things up quite a bit. EC: Very cutting-edge - but I think that's an adjective we've all come to associate with your name over time.  To that end, I was chatting with a colleague recently and your name came up in the conversation.  I told him that what amazed me was that you have not only taken a seemingly "boring" subject - nutrition - and made it "sexy" and "fun," but have actually done that for close to a decade now.  What's the secret to your success? JB:  Well, thanks for saying that, although I don't know if it's actually true.  However, if it is, it might be because of a few reasons. First, I can't tell you how many "nutrition experts" I've met that wouldn't know a healthy diet if it came up and bit them on the ear.  They may study nutrition.  And they may teach nutrition.  But they don't practice it.  And that's why they all seem to possess the same ability to make nutrition super-boring.  It's not real to them.  They don't live it day in and day out. On the other hand, I actually live the Precision Nutrition lifestyle.  365 days a year, I practice what I preach.  And, I've been doing exactly that for about 20 years now.  Plus, I've worked with a helluva lot of clients, at all levels.  So I pretty much practice nutrition and think about nutrition all the time.  Trust me, it makes a huge difference. EC: I can definitely attest to that.  Like you, I own my own business and have a lot of competing demands in my professional life, so it often seems that there aren't enough hours in the day.  In other words, working efficiently and having energy all the time is of paramount importance.  I've been following your work since the late 1990s and it's not only shaped my own personal nutrition practices, but also those of all of Cressey Performance's clients. JB:  And, you know, the funny thing is this.  When you do what I do, and you've done it for this long, you realize that there are a lot of nuances to eating well.  Sure, there's the what to eat, the when to eat, and the how much to eat.  And these are all very interesting.   But that's only scratching the surface. There's also the psychology of eating, which is quite fascinating.   There are genetic and individual differences associated with how each of us processes and tolerates foods.  And we haven't even mentioned supplements yet.  Nor have we talked about all the great new research that's coming out on food and nutrition every single day!  By exploring each of these very interesting areas, it's pretty easy to keep things fresh, new, and, hopefully exciting. EC: That's a good point. JB: Also, I always try to keep in mind that nutrition in the present deals in generalities.  There are recommended dietary intakes.  There are food pyramids.  There are general calculations for energy intake. However, nutrition is evolving in exciting ways.  It's becoming more individual.  And with blood analysis, genomic profiling, and more in the very near future, we'll be able to prescribe highly individualized nutrition plans for folks based on just a few simple tests. Indeed, the future is really exciting when it comes to nutrition.  And I'm happy that I'm in the prime of my career so I can ride the wave of this new nutrition information and technology. EC: Speaking of "evoluation," you've recently introduced Precision Nutrition: Version 3.0, which piggybacks on the first two installments.  What's new in this version? JB:  As our 46,000 members can attest to, I'm relentless about keeping the Precision Nutrition System, the cornerstone of all of our nutrition recommendations, up to date.


So, every year or two, we release a new version.  This time, it's our 3rd edition and this edition has improved upon V2 by an order of magnitude.  Now, don't get me wrong, V2 was great.  However, we've completely revised the content, we've added three new manuals/sections, and we've even given the whole project a facelift. As of V3, here's what folks can find:
  • The PN Success Guide
  • The PN Diet Guide
  • The Quick Start Guide
  • The Super Shake Guide
  • 5 Minute Meals
  • The Individualization Guide
  • The Measurement Guide
  • The Plant-Based Diet Guide (Brand New)
  • The Maintenance Guide (Brand New)
  • The Support Guide (Brand New)
In addition, we're now including Gourmet Nutrition V1, the Precision Nutrition Audio Collection, the Precision Nutrition Video Collection, and The Precision Nutrition Online Library.  It's a ton of great stuff.  Indeed, it's everything folks need to know to get the body they want. EC: Absolutely.  Thanks for helping out with the interview; sorry it took so long for us to make it happen! JB:  My pleasure.  Thanks, Eric. To find out more about Dr. John Berardi and his renowned Precision Nutrition System, head on over to PrecisionNutrition.com. Sign-up Today for our FREE Newsletter and receive a detailed deadlift technique tutorial!
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Weight Loss and Distance Running

It's that time of year in Boston.  The "shufflers" are out in full effect. For those of you who aren't familiar with a "shuffler," it's an individual who has recently taken up distance running as a means of losing weight.  As the weather gets nicer and the Boston Marathon rapidly approaches, you can spot shufflers out in droves all over Boston.  They shuffle for a number of reasons: 1. They believe that shuffling at 2.5mph is actually more effective than walking at 2.5mph. 2. Usually, they're about 80% of the way through the marathon training programs that were provided to them, and as a result, most are suffering from IT band problems, plantar fasciitis, Achilles and patellar tendinosis, sciatica, and a serious case of "whatthehellwasithinkingsigningupforthis-itis." 3. Because they never learned to sprint, they run with zero hip flexion (check out Newsletter 77: Sprinting for Health for details). 4. They are simply trying to finish their exercise in the most efficient way possible.  In other words, complete the task with as little discomfort as possible. And here, we have the problem.  Sally takes up running because she thinks she'll lose some body fat.  And, initially, she does lose weight because - to quote Alwyn Cosgrove - it's a "metabolic disturbance" compared to doing nothing.  Moving burns more calories than not moving. However, over time, that activity injures Sally and fosters bad movement patterns, meaning that she'll miss more exercise sessions down the road.  And, she quickly starts searching for the most efficient means of completing her runs, so her body gets more and more efficient - meaning that it burns fewer calories to accomplish the same task.  Whether it is three miles or 13 miles, it's always about just finishing.  Quantity always takes precedence over quality. With March Madness upon us, pretend you're watching a basketball game where you have two teams: Team A wants to win, and Team B wants to simply get through the 40 minutes of the game.  Team A dives for loose balls, full-court presses, and hits the boards hard.  Team B watches the clock.  Who burns more calories?  Team A, no doubt - because they get lost in their performance. Back in college, did you learn more in the graded courses, or the ones that were simply pass-fail?  And, as I asked in Maximum Strength, do you get stronger when you "train" or "work out?" This, to me, is one more reason why interval training outperforms steady-state cardio on top of all the other reasons (e.g., excess post-exercise oxygen consumption, reduction of overuse injuries) that we already know.  There is not a single effective exercise modality out there in a non-beginner population that works simply because one shows up and finishes.  The outstanding success loads of folks have had with Warpspeed Fat Loss is a perfect example; Cosgrove and Mike Roussell challenged them to be just a little bit better at each successive training session - either with loading or number of sets completed.


If you are going to distance-run (and aren't a competitive endurance athlete), focus on going faster, not fine-tuning the art of pacing yourself when grandmothers are passing you with their walkers.  Pacing yourself doesn't even work at all-you-can-eat buffets; everyone knows you get full too fast and never live up to your gluttony potential.  And, as I always say, if it doesn't fly at all-you-can-eat buffets, it just ain't right. If you're going to interval train, your goal is to go faster each time.  More watts, more steps in a given time period, more ghastly stares from the lady reading a magazine on the leg press, whatever.  Mike Boyle had some great thoughts on this front in a recent submission HERE.  As long as it is quantifiable and you're busting your hump to compete against your previous best, I'm happy. I like the idea of camaraderie and/or competition with others in interval training, too. For example, our staff did this 16-yard x 16-trip sled medley three Thursdays in a row - and each time, it was a little faster (meaning that we had fewer rest periods between sets):

Later in the week, I'll be back with more thoughts to keep this headed in the right direction. New Blog Content Random Friday Thoughts Barefoot Training Guidelines Big Bench to Bigger Bench Stuff You Should Read All the Best, EC

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A Win/Win: Drop 10lbs or Make $20

Just a quick heads-up for my readers on a great offer that's available for a short amount of time... As you know, I'm a big fan of Alwyn Cosgrove and Mike Roussell's Warpspeed Fat Loss program.  It's an extremely comprehensive and effective fat loss protocol I've seen work wonders with some of our clients, staff members (myself included), and even my girlfriend.  I even wrote up two newsletters (here and here) about the amazing results one of our clients had with it. Anyway, Alwyn and Mike are guaranteeing that their product will take ten pounds off you in 28 days or else they'll refund your money plus $20 for your time and effort.  They're only making this available to the first 100 people, though.  And, even if they don't sell 100, it'll be taken down on Monday - so don't wait! Click here to check out this sweet offer.


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Triple Threat?

One of the pro baseball guys I work with from afar is in town this week for a check-in, and he bought ten protein bars for $10 in anticipation of eating out of airports.  He was munching on one of them at the facility yesterday, and it was labeled as a "Triple Threat" for a) great taste, b) energy, and c) nutrition. Now, you're talking to a guy who spent two years at business school before deciding to go the exercise science route, so I've got a little marketing analyst in me.  We all know that lots of stuff can have double meanings - so I check out the first three ingredients: 1. Corn Syrup 2. Soy Crisps 3. "Chocolatey" Coating Yes, it really had a "Y" on the end of the word.  So, you not get a candy bar with crap ingredients, but also are treated like a child with words like "chocolatey." Joking aside, the best protein bars available are the ones you make yourself.  John Berardi has some awesome recipes in Gourmet Nutrition Cookbook (also available as part of the Precision Nutrition package).


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Understanding Insulin

Understanding Insulin

By: Eric Cressey

All too often, we overlook the important underlying anatomy and physiology upon which solid training and nutrition recommendations are based. In rushing to get to the "meat and potatoes" (the program or ultimate recommendations) of an article, we fail to truly question and understand the basis for why we do what we do. Take, for example, post-workout nutrition. Ever wonder why you can suck up ridiculous amounts of high-carb foods after you train? In the Rugged mission statement, we promised to make you think; the following article should do just that. And, if it doesn't, you can at least gain an appreciation for one facet of an Exercise Science graduate student's course of study. Without further ado, I present "the insulin response to exercise: carbohydrate, fat, and protein metabolism implications." Introduction Insulin is well recognized as a powerful hormone capable of diverse metabolic effects in a variety of scenarios. Perhaps the most noteworthy of these scenarios is exercise, the stress of which presents significant metabolic demands. The response of insulin to these demands has far-reaching implications in terms of carbohydrate, fat, and protein metabolism. Insulin: Broad Roles in Carbohydrate, Fat, and Protein Metabolism Insulin exerts its most pronounced effects on carbohydrate metabolism at the skeletal muscle and hepatic levels. The hormone facilitates uptake of glucose into skeletal muscle and the liver, thus promoting glycogenesis. Simultaneously, it inhibits hepatic glucose release (glycogenolysis) and production (gluconeogenesis) (1). Insulin appears to demonstrate its most immediate and powerful influence in suppressing glycogenolysis, as more insulin is required to inhibit gluconeogenesis than glycogenolysis in non-diabetic subjects (2). Insulin also plays crucial roles in fat metabolism, regulating both lipolysis and lipogenesis. Lipolysis, the hydrolysis of triglycerides, is a requisite step in fat oxidation, as it liberates fatty acids for transport to mitochondria for oxidation (3). Numerous studies have demonstrated that insulin markedly blunts lipolysis at rest (3-5). Likewise, via facilitation of glucose uptake in liver and adipose tissue, insulin stimulates lipogenesis as well. Glycolytic conversion of glucose to acetyl-CoA is the precursor to fatty acid synthesis (1,6). In terms of protein metabolism, insulin's foremost role is inhibition of protein breakdown. Although the hormone does play a role in promoting protein synthesis, this effect is largely dependent on amino acid availability (7-9). Some studies have noted that insulin elevations without concurrent increases in amino acid availability actually decrease protein synthesis as a result of low plasma amino acid concentrations (10,11). Conversely, dietary amino acids exert their most prominent effect on optimizing protein synthesis rather than reducing protein breakdown (7,8,12). Hormonal Regulation of Blood Glucose: Carbohydrate, Fat, and Protein Metabolism Maintenance of plasma glucose concentrations is of paramount importance to optimal functioning of muscles and the central nervous system. Blood glucose regulation involves interactions of carbohydrate, fat, and protein metabolism; these interactions are even more readily apparent during exercise. While insulin is certainly a powerful modulator of plasma glucose levels, one must also consider several other hormones that exert the opposite physiological effects as insulin. Knowledge of these hormones - glucagon, growth hormone, cortisol, and the catecholamines epinephrine and norepinephrine - is an important prerequisite to comprehending the insulin response to exercise. Glucagon responds to the same stimuli as insulin, but has the exact opposite effects on blood glucose concentrations. These effects are, on the whole, catabolic and anti-anabolic. They include stimulation of glycogenolysis, gluconeogenesis, and protein degradation with concurrent inhibition of protein synthesis (13,14). Some studies have noted that glucagon has a stimulatory effect on lipolysis in human adipose tissue in vitro, and pharmacological interventions to induce dramatic hyperglucagonemia have proven sufficient to stimulate lipolysis (15-17). However, there is insufficient evidence to suggest that normal human hyperglucagonemia can directly induce lipolysis in vivo (18,19). While hypoglycemia is the most potent stimuli for glucagon release from the pancreas, high concentrations of insulin during hypoglycemia can suppress the glucagon response (20). Growth hormone serves as a counter-regulatory hormone to insulin in carbohydrate and fat metabolism, but works synergistically with insulin in establishing an anabolic protein metabolism environment (21). Growth hormone's insulin-antagonistic effects include increased lipolysis, decreased tissue glucose uptake, and enhanced hepatic gluconeogenesis (22-24). Meanwhile, growth hormone has an anabolic effect via enhanced protein synthesis and retention (25-31). Cortisol opposes insulin action in several regards. This glucocorticoid is likely most well known for its catabolic properties, which include stimulation of lipolysis in adipose tissue, protein degradation (the hormone also inhibits protein synthesis), and hepatic gluconeogenesis (32-35). Additionally, in terms of insulin resistance, cortisol not only directly inhibits glucose entry to cells, but also delays insulin action via a post-insulin receptor block (33,36). The catecholamines epinephrine and norepinephrine work in opposition to insulin in the regulation of the plasma glucose concentration. Epinephrine provides a strong stimulus to hepatic glucose mobilization via glycogenolysis and gluconeogenesis (37), although there is a lower threshold for glycogenolysis to occur (38). The catecholamines also stimulate lipolysis in adipose tissue (33,39) and interfere with glucose clearance by insulin (40). While the catecholamines have a catabolic effect on both liver and skeletal muscle glycogen, there is considerable evidence that they have anti-catabolic effects on muscle protein (41-43). Thyroxine is a less recognized regulator of plasma glucose concentrations. While the hormone itself has no direct effect on substrate mobilization at rest or during exercise, it does serve a permissive role for the hormones that are directly involved in plasma glucose regulation. Thyroxine acts by either increasing receptor quantity at the target tissues or by increasing receptor affinity for the aforementioned hormones; during exercise, these effects are more pronounced, as there is an increase in free thyroxine concentrations (33). Hypothyroidism (and the related thyroxine deficiency) has been shown to interfere with fuel mobilization (33). Clearly, a discussion of insulin must include attention to several glucoregulatory hormones, each of which has significant implications in carbohydrate, fat, and protein metabolism. Figure 1 summarizes the roles of those hormones with a direct effect on fuel metabolism in the liver, skeletal muscle, and adipose tissue.


Glucoregulatory Hormone Response to Exercise Insulin is the only glucoregulatory hormone that decreases with exercise under normal physiologic conditions (33). Galbo et al. (1975) found that insulin decreased both during prolonged treadmill running at 76%VO2max and with incremental treadmill exercise at 47% and 77% VO2max (no significant difference was noted at 100% VO2max) (44). Numerous other studies have observed similar decreases (45-47); these decreases are more prominent in longer duration exercise at lower intensities than in short duration, high intensity exercise (47). As a hormone working in direct opposition to insulin, glucagon increases in response to exercise. This effect has been demonstrated in both incremental (44) and prolonged (44,45) endurance exercise. In the aforementioned study by Galbo et al. (1975), the investigators found that glucagon increased more in the longer duration scenario (threefold increase over the resting value) than in incremental exercise (an increase of 35% from rest to VO2max) (44). Others have also noted that glucagon's effects are clearly more prominent in longer duration scenarios (48). Describing plasma growth hormone changes during exercise proves to be a complex task, as numerous physical, psychological, chemical, and exercise modality (both aerobic and resistance training) factors. In a broad sense, plasma growth hormone concentrations increase as exercise intensity increases; plasma GH may increase 25-fold over resting concentrations at VO2max (49). In fact, recent research by Wideman et al. (2003) noted a linear relationship between GH secretion and exercise intensity (50). Bunt et al. (1986) found that plasma GH increased by 500-600% in both runners and non-runners (runners had a higher response) during one hour of treadmill running at 60% VO2max, implying a duration effect for GH secretion as well (33,51). The growth hormone response to resistance training is a product of the work-rest intervals, loads, and volume utilized, with one minute rest periods, 10-repetition maximums, and high volumes proving most beneficial in enhancing GH secretion (50,52). Cortisol increases in response to exercise are related to intensity and duration. A study by Davies and Few (1973) demonstrated the presence of an intensity threshold that must be reached for cortisol increases to occur. In separate exercise sessions, subjects were tested for 60 minutes at 40%, 60%, 80%, and 100% VO2max. Plasma cortisol actually decreased at 40% VO2max over the course of the test, whereas cortisol increased whenever the intensity exceeded 60% VO2max (33). Apparently, light exercise facilitates plasma cortisol removal to the point that it exceeds secretion by the adrenal cortex in response to exercise. At greater intensities, secretion predominated over removal, which had increased even more (33). There also appears to be a duration threshold; Bonen (1973) observed that urinary excretion of cortisol did not change with 10 minutes of exercise at 76% VO2max. However, when the duration increased to 30 minutes, this excretion value doubled (53), likely due to a lag time in the hypothalamic-pituitary-adrenal axis between ACTH and cortisol secretion (54). Numerous studies have found that epinephrine and norepinephrine secretions increase as exercise intensity increases (55-58). However, Kraemer et al. (1985) found that graded exercise did not increase plasma epinephrine above baseline at 54% VO2 max, implying an intensity threshold for catecholamine secretion (59). Several investigators have observed increasing plasma catecholamine concentrations as exercise duration increased (60,61). Galbo et al. (1975) demonstrated that intensity is more influential than duration in the catecholamine response to exercise, as plasma epinephrine increased steadily with prolonged treadmill exercise to exhaustion at 76% VO2 max, but graded exercise in the same subjects at 44, 77, and 100% of VO2 max yielded greater increases (55). Glucose Uptake and Transport during Exercise During exercise, muscle glucose uptake may increase 30-50 fold over resting values (62). There is only a limited supply of muscle glycogen, and it can virtually be depleted with just one hour of exercise at 70-75% VO2max (63); therefore, it is of no surprise that muscle glucose uptake increases so dramatically. Given insulin's key role in promoting glucose uptake in skeletal muscle, it seems counterintuitive that the hormone would actually decrease with exercise. However, numerous physiological factors interact to ensure that plasma glucose is maintained while skeletal muscles receive adequate fuel for the continuation of exercise. First, and perhaps most logically, muscular contractions promote blood flow to skeletal muscles. With blood flow comes more glucose and insulin, so in spite of the fact that insulin is actually decreasing, there is still more opportunity for glucose uptake than at rest (33,64). Meanwhile, a gradient for more rapid glucose diffusion into the cell via increased membrane permeability is created because the muscles are utilizing glucose at a faster rate (64,65). Like insulin, exercise also leads to glucose transporter changes at the sarcolemmal level. In both scenarios, membrane transport capability increases due to translocation of insulin-stimulated GLUT4 transporters to the sarcolemma and transverse tubules from intracellular sites (65-69). Kennedy et al. (1999) demonstrated that 45-60 minutes of bicycling at 60-75% VO2max resulted in acute mean increases of 71-74% in sarcolemmal GLUT4 content in both normal and type 2 diabetic subjects (70). Others have verified this increase in plasma membrane GLUT4 content with exercise (71-73). The mechanism by which muscle contraction facilitates GLUT4 translocation to the plasma membrane is yet to be definitively elucidated; however, the most likely answer is high intramuscular calcium concentrations during exercise. More specifically, protein kinase C (PKC) is an intermediary that is dependent on calcium; PKC downregulation has been associated with reduced contraction-induced glucose transport (33,73). Potential autocrine and paracrine effects on contraction-stimulated glucose transport have also been suggested (73). You can find a scheme of the potential factors influencing GLUT4 translocation in skeletal muscle here (Hayashi et al, Am J Physiol 1997). For the sake of this discussion, it is important to note that insulin and muscular contraction facilitate glucose transport via different pathways, as Yeh et al. (1995) noted that it is possible to inhibit insulin action without inhibiting that of muscle contractions (74). Brozinick et al. (1992) validated this assertion with the observation that contraction-induced facilitated glucose transport is normal in insulin resistant muscle (75). GLUT4 and GLUT1 are two key glucose transporters found in skeletal muscle. Unlike GLUT4, which is responsive to insulin action, GLUT1 exerts its effects on glucose transport independent of insulin stimulation (69). Henriksen et al. (1990) observed that GLUT4 protein concentration is closely associated with maximal glucose transport capability; it logically follows that the overall quantity of glucose transporters (both GLUT4 and GLUT1) in the plasma membrane during exercise is proportional to muscle GLUT4 content (76). However, there is evidence to suggest that GLUT4 transporters are more associated with fast-twitch oxidative-glycolytic fibers, while GLUT1 transporters are associated with slow-twitch oxidative fibers. Additionally, there is evidence to suggest that GLUT1 transporter increases are achieved through several weeks of endurance training, whereas GLUT4 transporters are more responsive to individual exercise bouts (77). Therefore, variations in fiber-type may interfere with this assumption (78). Summarily, with more glucose transporters (both insulin-stimulated and non-insulin-stimulated) present due to both chronic and acute exercise adaptations, less insulin is necessary to have the same physiological effect. On a related note, Ivy (1997) asserted that increased concentrations of enzymes responsible for the phosphorylation, storage, and oxidation of glucose are also responsible for the improved insulin action (68). Conclusions: Bringing it all Together At first glance, it seems counterintuitive for insulin to decrease during exercise, a time when muscle glucose uptake increases rapidly. Upon further review, though, one can recognize that numerous hormonal and intracellular factors interact with this decrease to maintain plasma glucose concentrations, facilitate muscle glucose uptake, and effect appropriate changes in carbohydrate, fat, and protein metabolism. As exercise progresses, skeletal muscle glycogen depletion occurs and the muscles must look to plasma glucose as a fuel source. Assuming no provision of exogenous carbohydrate during exercise, plasma glucose must come from hepatic gluconeogenesis or glycogenolysis. These physiological occurrences are stimulated by the presence of the glucagon, epinephrine, and norepinephrine at the onset of exercise, and growth hormone and cortisol as exercise duration increases (33). As counterregulators to insulin, these five hormones can only be present in sufficient quantities to elicit the desirable effects on plasma glucose maintenance if the plasma insulin concentration is low. While the counterregulatory hormones take care of maintaining plasma glucose, there must be additional physiological adaptations to promote muscle glucose uptake in spite of the decrease in plasma insulin concentrations that occur with exercise. These exercise-induced physiological adaptations include increased skeletal muscle blood flow (and, in turn, glucose and insulin delivery), increased membrane permeability to glucose, translocation of GLUT4 proteins to the sarcolemma and transverse tubules, and increased cellular concentrations of key enzymes involved in glucose utilization. While both insulin and exercise favorably influence glucose uptake, they do so by different pathways. Nonetheless, the positive effects of acute and chronic exercise on insulin action and both insulin-dependent and non-insulin-dependent glucose transporters are undeniable. It is important to also note that glucagon, growth hormone, cortisol, and the catecholamines have effects that extend beyond plasma glucose regulation. All five hormones promote lipolysis, and thus serve as powerful regulators of fat metabolism (which is also dependent on insulin-related lipogenesis). This increased lipolysis favors the increased reliance on free fatty acids with longer durations, lower intensities, and situations of muscle glycogen depletion (79-82). Likewise, some of these hormones - glucagon, the catecholamines, and most notably, cortisol - continue to oppose insulin in protein metabolism by promoting proteolysis and inhibiting protein synthesis. Meanwhile, growth hormone works synergistically with insulin (and amino acids) to achieve an anabolic effect of elevated protein synthesis and decreased protein breakdown. References 1. Khan AH, Pessin JE. Insulin regulation of glucose uptake: a complex interplay of intracellular signalling pathways. Diabetologia. 2002 Nov;45(11):1475-83. Epub 2002 Oct 18. 2. Adkins A, Basu R, Persson M, Dicke B, Shah P, Vella A, Schwenk WF, Rizza R. Higher insulin concentrations are required to suppress gluconeogenesis than glycogenolysis in nondiabetic humans. Diabetes. 2003 Sep;52(9):2213-20. 3. Horowitz JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol. 1997 Oct;273(4 Pt 1):E768-75. 4. Bonadonna RC, Groop LC, Zych K, Shank M, DeFronzo RA. Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans. Am J Physiol. 1990 Nov;259(5 Pt 1):E736-50. 5. Campbell PJ, Carlson MG, Hill JO, Nurjhan N. Regulation of free fatty acid metabolism by insulin in humans: role of lipolysis and reesterification. Am J Physiol. 1992 Dec;263(6 Pt 1):E1063-9. 6. Kersten S. Mechanisms of nutritional and hormonal regulation of lipogenesis. EMBO Rep. 2001 Apr;2(4):282-6. 7.Castellino P, Luzi L, Simonson DC, Haymond M, DeFronzo RA. Effect of insulin and plasma amino acid concentrations on leucine metabolism in man. Role of substrate availability on estimates of whole body protein synthesis. J Clin Invest. 1987 Dec;80(6):1784-93. 8.Tessari P, Inchiostro S, Biolo G, Trevisan R, Fantin G, Marescotti MC, Iori E, Tiengo A, Crepaldi G. Differential effects of hyperinsulinemia and hyperaminoacidemia on leucine-carbon metabolism in vivo. Evidence for distinct mechanisms in regulation of net amino acid deposition. J Clin Invest. 1987 Apr;79(4):1062-9. 9. Heslin MJ, Newman E, Wolf RF, Pisters PW, Brennan MF. Effect of hyperinsulinemia on whole body and skeletal muscle leucine carbon kinetics in humans. Am J Physiol. 1992 Jun;262(6 Pt 1):E911-8. 10. McNurlan MA, Garlick PJ. Influence of nutrient intake on protein turnover. Diabetes Metab Rev. 1989 Mar;5(2):165-89. 11. Frexes-Steed M, Lacy DB, Collins J, Abumrad NN. Role of leucine and other amino acids in regulating protein metabolism in vivo. Am J Physiol. 1992 Jun;262(6 Pt 1):E925-35. 12. Svanberg E, Moller-Loswick AC, Matthews DE, Korner U, Andersson M, Lundholm K. Effects of amino acids on synthesis and degradation of skeletal muscle proteins in humans. Am J Physiol. 1996 Oct;271(4 Pt 1):E718-24. 13. Gravholt CH, Moller N, Jensen MD, Christiansen JS, Schmitz O. Physiological levels of glucagon do not influence lipolysis in abdominal adipose tissue as assessed by microdialysis. J Clin Endocrinol Metab. 2001 May;86(5):2085-9. 14. Charlton MR, Adey DB, Nair KS. Evidence for a catabolic role of glucagon during an amino acid load. J Clin Invest. 1996 Jul 1;98(1):90-9. 15. Liljenquist JE, Bomboy JD, Lewis SB, et al. 1974 Effects of glucagon on lipolysis and ketogenesis in normal and diabetic men. J Clin Invest. 53:190?197. 16. Gerich JE, Lorenzi M, Bier DM, et al. 1976 Effects of physiologic levels of glucagon and growth hormone on human carbohydrate and lipid metabolism. Studies involving administration of exogenous hormone during suppression of endogenous hormone secretion with somatostatin. J Clin Invest. 57:875?884. 17. Schneider SH, Fineberg SE, Blackburn GL. 1981 The acute metabolic effects of glucagon and its interactions with insulin in forearm tissue. Diabetologia. 20:616?624. 18. Carlson MG, Snead WL, Campbell PJ. 1993 Regulation of free fatty acid metabolism by glucagon. J Clin Endocrinol Metab. 77:11?15. 19. Jensen MD, Heiling VJ, Miles JM. 1991 Effects of glucagon on free fatty acid metabolism in humans. J Clin Endocrinol Metab. 72:308?315. 20. Liu D, Moberg E, Kollind M, Lins PE, Adamson U. A high concentration of circulating insulin suppresses the glucagon response to hypoglycemia in normal man. J Clin Endocrinol Metab. 1991 Nov;73(5):1123-8. 21. Moller N, Jorgensen JO, Abildgard N, Orskov L, Schmitz O, Christiansen JS. Effects of growth hormone on glucose metabolism. Horm Res. 1991;36 Suppl 1:32-5. 22. Jorgensen JOL, Møller J, Alberti KG, et al. Marked effects of sustained low growth hormone (GH) levels on day-to-day fuel metabolism: studies in GH-deficient patients and healthy untreated subjects. J Clin Endocrinol Metab. 1993;77:1589?1596. 23. Moller N, Schmitz O, Pørksen N, Møller J, Jørgensen JOL. Dose-response studies on the metabolic effects of a growth hormone pulse in humans. Metabolism. 1992;41:172?175. 24. Fowelin J, Attvall S, von Schenck H, Smith U, Lager I. Characterization of the insulin-antagonistic effect of growth hormone in man. Diabetologia. 1991;34:500?506. 25. Moller N, Norrelund H. The role of growth hormone in the regulation of protein metabolism with particular reference to conditions of fasting. Horm Res. 2003;59 Suppl 1:62-8. 26. Clemmons DR, Snyder DK, Williams R, Underwood LE: Growth hormone administration conserves lean body mass during dietary restriction in obese subjects. J Clin Endocrinol Metab 1987;64:878-883. 27. Gamrin L, Essen P, Hultman E, McNurlan MA, Garlick PJ, Wernerman J. Protein-sparing effect in skeletal muscle of growth hormone treatment in critically ill patients. Ann Surg. 2000 Apr;231(4):577-86. 28. Lundeberg S, Belfrage M, Wernerman J, von der Decken A, Thunell S, Vinnars E: Growth hormone improves muscle protein metabolism and whole body nitrogen economy in man during a hyponitrogenous diet. Metabolism 1991;40:315-322. 29. Carli F, Webster JD, Halliday D: Growth hormone modulates amino acid oxidation in the surgical patient: leucine kinetics during the fasted and fed state using moderate nitrogenous and caloric diet and recombinant human growth hormone. Metabolism 1997;46:23-28. 30. Copeland KC, Nair KS: Acute growth hormone effects on amino acid and lipid metabolism. J Clin Endocrinol Metab 1994;78:1040-1047. 31. Fryburg DA, Barrett EJ: Growth hormone acutely stimulates skeletal muscle but not whole-body protein synthesis in humans. Metabolism 1993;42:1223-1227. 32. Divertie GD, Jensen MD, Miles JM. Stimulation of lipolysis in humans by physiological hypercortisolemia. Diabetes. 1991 Oct;40(10):1228-32. 33. Powers, SK, Howley, ET. Exercise physiology, 4th edition. Boston: McGraw Hill, 2001. 34. Brillon DJ, Zheng B, Campbell RG, Matthews DE. Effect of cortisol on energy expenditure and amino acid metabolism in humans. Am J Physiol. 1995 Mar;268(3 Pt 1):E501-13. 35. Simmons PS, Miles JM, Gerich JE, Haymond MW. Increased proteolysis. An effect of increases in plasma cortisol within the physiologic range. J Clin Invest. 1984 Feb;73(2):412-20. 36. Rizza RA, Mandarino LJ, Gerich JE. Cortisol-induced insulin resistance in man: impaired suppression of glucose production and stimulation of glucose utilization due to a postreceptor detect of insulin action. J Clin Endocrinol Metab. 1982 Jan;54(1):131-8. 37. Sherwin RS, Sacca L. Effect of epinephrine on glucose metabolism in humans: contribution of the liver. Am J Physiol. 1984 Aug;247(2 Pt 1):E157-65. 38. Sacca L, Vigorito C, Cicala M, Corso G, Sherwin RS. Role of gluconeogenesis in epinephrine-stimulated hepatic glucose production in humans. Am J Physiol. 1983 Sep;245(3):E294-302. 39. Cryer PE. Adrenaline: a physiological metabolic regulatory hormone in humans? Int J Obes Relat Metab Disord. 1993 Dec;17 Suppl 3:S43-6; discussion S68. 40. Rizza R, Haymond M, Cryer P, Gerich J. Differential effects of epinephrine on glucose production and disposal in man. Am J Physiol. 1979 Oct;237(4):E356-62. 41. Fryburg DA, Gelfand RA, Jahn LA, Oliveras D, Sherwin RS, Sacca L, Barrett EJ. Effects of epinephrine on human muscle glucose and protein metabolism. Am J Physiol. 1995 Jan;268(1 Pt 1):E55-9. 42. Miles JM, Nissen SL, Gerich JE, Haymond MW. Effects of epinephrine infusion on leucine and alanine kinetics in humans. Am J Physiol. 1984 Aug;247(2 Pt 1):E166-72. 43. Kraenzlin ME, Keller U, Keller A, Thelin A, Arnaud MJ, Stauffacher W. Elevation of plasma epinephrine concentrations inhibits proteolysis and leucine oxidation in man via beta-adrenergic mechanisms. J Clin Invest. 1989 Aug;84(2):388-93 44. Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol. 1975 Jan;38(1):70-6. 45. Miller SL, Maresh CM, Armstrong LE, Ebbeling CB, Lennon S, Rodriguez NR. Metabolic response to provision of mixed protein-carbohydrate supplementation during endurance exercise. Int J Sport Nutr Exerc Metab. 2002 Dec;12(4):384-97. 46. Bonen A, Belcastro AN, MacIntyre K, Gardner J. Hormonal responses during intense exercise preceded by glucose ingestion. Can J Appl Sport Sci. 1980 Jun;5(2):85-90. 47. Tatar P, Kozlowski S, Vigas M, Nazar K, Kvetnansky R, Jezova D, Kaciuba-Uscilko H. Endocrine response to physical efforts with equivalent total work loads but different intensities in man. Endocrinol Exp. 1984 Dec;18(4):233-9. 48. Kjaer M. Hepatic glucose production during exercise. Adv Exp Med Biol. 1998;441:117-27. 49. Sutton J, Lazarus L. Growth hormone in exercise: comparison of physiological and pharmacological stimuli. J Appl Physiol. 1976 Oct;41(4):523-7. 50. Wideman L, Weltman JY, Hartman ML, Veldhuis JD, Weltman A. Growth hormone release during acute and chronic aerobic and resistance exercise: recent findings. Sports Med. 2002;32(15):987-1004. 51. Bunt JC, Boileau RA, Bahr JM, Nelson RA. Sex and training differences in human growth hormone levels during prolonged exercise. J Appl Physiol. 1986 Nov;61(5):1796-801. 52. Baechle, TR, Earle, RW. Essentials of Strength and Conditioning, 2nd edition. Champaign, IL: Human Kinetics, 2001. 53. Bonen A. Effects of exercise on excretion rates of urinary free cortisol. J Appl Physiol. 1976 Feb;40(2):155-8. 54. Rasmuson S, Olsson T, Hagg E. A low dose ACTH test to assess the function of the hypothalamic-pituitary-adrenal axis. Clin Endocrinol (Oxf). 1996 Feb;44(2):151-6. 55. Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol. 1975 Jan;38(1):70-6. 56. de Diego Acosta AM, Garcia JC, Fernandez-Pastor VJ, Peran S, Ruiz M, Guirado F. Influence of fitness on the integrated neuroendocrine response to aerobic exercise until exhaustion. J Physiol Biochem. 2001 Dec;57(4):313-20. 57. Kraemer WJ, Dziados JE, Gordon SE, Marchitelli LJ, Fry AC, Reynolds KL. The effects of graded exercise on plasma proenkephalin peptide F and catecholamine responses at sea level. Eur J Appl Physiol Occup Physiol. 1990;61(3-4):214-7. 58. McMurray RG, Forsythe WA, Mar MH, Hardy CJ. Exercise intensity-related responses of beta-endorphin and catecholamines. Med Sci Sports Exerc. 1987 Dec;19(6):570-4. 59. Kraemer WJ, Noble B, Culver B, Lewis RV. Changes in plasma proenkephalin peptide F and catecholamine levels during graded exercise in men. Proc Natl Acad Sci U S A. 1985 Sep;82(18):6349-51. 60. Sothmann MS, Blaney J, Woulfe T, Donahue-Fuhrman S, Lefever K, Gustafson AB, Murthy VS. Plasma free and sulfoconjugated catecholamines during sustained exercise. J Appl Physiol. 1990 Feb;68(2):452-6. 61. Rostrup M, Westheim A, Refsum HE, Holme I, Eide I. Arterial and venous plasma catecholamines during submaximal steady-state exercise. Clin Physiol. 1998 Mar;18(2):109-15. 62. Sahlin K. Muscle glucose metabolism during exercise. Ann Med. 1990 Jun;22(3):85-9. 63. Coggan AR, Coyle EF. Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. Exerc Sport Sci Rev. 1991;19:1-40. 64. Ivy JL. The insulin-like effect of muscle contraction. Exerc Sport Sci Rev. 1987;15:29-51. 65. Wojtaszewski JF, Richter EA. Glucose utilization during exercise: influence of endurance training. Acta Physiol Scand. 1998 Mar;162(3):351-8. 66. Richter EA, Kristiansen S, Wojtaszewski J, Daugaard JR, Asp S, Hespel P, Kiens B. Training effects on muscle glucose transport during exercise. Adv Exp Med Biol. 1998;441:107-16. 67. Goodyear LJ, Kahn BB. Exercise, glucose transport, and insulin sensitivity. Annu Rev Med. 1998;49:235-61. 68. Ivy JL. Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med. 1997 Nov;24(5):321-36. 69. Ivy JL, Kuo CH. Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise. Acta Physiol Scand. 1998 Mar;162(3):295-304. 70. Kennedy JW, Hirshman MF, Gervino EV, Ocel JV, Forse RA, Hoenig SJ, Aronson D, Goodyear LJ, Horton ES. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Diabetes. 1999 May;48(5):1192-7. 71. Douen AG, Ramlal T, Rastogi S, Bilan PJ, Cartee GD, Vranic M, Holloszy JO, Klip A. Exercise induces recruitment of the "insulin-responsive glucose transporter". Evidence for distinct intracellular insulin- and exercise-recruitable transporter pools in skeletal muscle. J Biol Chem. 1990 Aug 15;265(23):13427-30. 72. Fushiki T, Wells JA, Tapscott EB, Dohm GL. Changes in glucose transporters in muscle in response to exercise. Am J Physiol. 1989 May;256(5 Pt 1):E580-7. 73. Hayashi T, Wojtaszewski JF, Goodyear LJ. Exercise regulation of glucose transport in skeletal muscle. Am J Physiol. 1997 Dec;273(6 Pt 1):E1039-51. 74. Yeh JI, Gulve EA, Rameh L, Birnbaum MJ. The effects of wortmannin on rat skeletal muscle. Dissociation of signaling pathways for insulin- and contraction-activated hexose transport. J Biol Chem. 1995 Feb 3;270(5):2107-11. 75. Brozinick JT Jr, Etgen GJ Jr, Yaspelkis BB 3rd, Ivy JL. Contraction-activated glucose uptake is normal in insulin-resistant muscle of the obese Zucker rat. J Appl Physiol. 1992 Jul;73(1):382-7. 76. Henriksen EJ, Bourey RE, Rodnick KJ, Koranyi L, Permutt MA, Holloszy JO. Glucose transporter protein content and glucose transport capacity in rat skeletal muscles. Am J Physiol. 1990 Oct;259(4 Pt 1):E593-8. 77. Phillips, S., et al. Increments in skeletal muscle GLUT-1 and GLUT-4 after endurance training in humans. Am J Physiol. 1996 Mar;270(3 Pt 1):E456-62. 78. Johannsson, E., Effect of cross-reinnervation on the expression of GLUT-4 and GLUT-1 in slow and fast rat muscles. Am J Physiol. 1996 Jun;270(6 Pt 2):R1355-60. 79. Holloszy JO, Kohrt WM, Hansen PA. The regulation of carbohydrate and fat metabolism during and after exercise. Front Biosci. 1998 Sep 15;3:D1011-27. 80. Jensen MD. Fate of fatty acids at rest and during exercise: regulatory mechanisms. Acta Physiol Scand. 2003 Aug;178(4):385-90. 81. Spriet LL, Watt MJ. Regulatory mechanisms in the interaction between carbohydrate and lipid oxidation during exercise. Acta Physiol Scand. 2003 Aug;178(4):443-52. 82.Coggan AR. Plasma glucose metabolism during exercise in humans. Sports Med. 1991 Feb;11(2):102-24.
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Random Friday Thoughts: 12/5/2008

1.  I have seen a lot of guys who have hamstrings pulls in their health histories, but I don't recall ever coming across any studies that show that shooting yourself in the leg expedites recovery time.

The sad truth is that you'll probably have dozens of kids around the country with hamstrings strains shoot themselves in the leg in hopes of returning to play sooner because "Burress does it."  I'll stick with soft tissue work, glute activation, and sprint mechanics training... 2. I got a question the other day about how we approach rest periods for our medicine ball work, and while it could be somewhat of a long, detailed response, I can probably respond even better with a simple, "We are always trying to slow guys down because they rush through them."  Usually, our rest intervals are in the ballpark of one minute between sets.  So, here's a little sample of what one of our professional pitchers did yesterday: A) Side High Box Step-ups w/Leg Kick: 2x4/side B1) Overhead Med Ball Stomp to Floor: 4x8 (5kg) B2) Side-Lying Extension-Rotation: 3x8/side C1) Recoiled Shotput: 3x3/side (4kg) C2) Wall Hip Flexor Mobilizations: 2x8/side D1) Recoiled Shotput: 3x3/side (2kg) D2) Lying Knee-to-Knee Stretch: 2x30s E1) Crow Hop to Overhead Med Ball Throw: 5x2 (2kg) E2) Multiplanar Hamstrings Mobilizations: 2x5/5/5/side So, as you can see, we use mobility work between sets to slow the guys down and address range-of-motion deficits they might have at the same time.  A lot of these drills can be found on Magnificent Mobility (lower body) and Inside-Out (upper body).

3. It was a wild Thanksgiving morning at Cressey Performance; we had ten people in to train and get after it with the staff.  For some great commentary, check out these two posts: Tony Gentilcore: First Annual Cressey Performance Thanksgiving Morning Lift Steph Holland-Brodney: Testosterone, Training, Talk, and Turkey: My Thanksgiving Thursday Who needs Turkey Trots when you can just do 405x20 on the trap bar and get it over with?

4. For some good reading - particularly with respect to nutrition - check out Brian St. Pierre's blog. 5. I'm going with Joseph Addai over LenDale White this weekend.  Thanks to everyone for the feedback from Tuesday.  Fingers crossed... 6. Happy Birthday to Cassandra Forsythe-Pribanic!  Cass and I go way back, and she's been a great friend and resource for me all along the way.  If you're looking for top-notch female-specific nutrition and fitness resources, you definitely ought to check out The New Rules of Lifting for Women and the Women's Health Perfect Body Diet, both of which Cass or co-authored.

That'll do it for this week.  I've got some sweet content in line for next week, so stay tuned.  Have a great weekend!
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FFL Week 12: Greg Tops Gregg

I knocked off Gregg T. this week in fantasy football, 84-56, to bring my winning streak to three and catapult (yes, it was that dramatic) myself into a three-way tie for second place in our league at 7-5.  It was pretty redeeming, as Gregg talked a lot of smack a few weeks ago when he heard that I was terrible at bowling. You see, Gregg's bowled a few 800+ games (he defies conventional bowling scoring systems) and has enjoyed all the fame and fortune that goes along with dominating in a sport with so much international acclaim.  In fact, each time he walked from the car to Cressey Performance to train, he was swarmed by adoring fans.  He'd usually walk in the door, gather up all the women's underwear that had been thrown at him, sign a few autographs, and then get his lift on. This week however, Gregg T. was outdone by Greg J - Jennings, that is.  If you didn't see it, Jennings (a Green Bay WR who carried my team this week) put on a show last night in spite of his team getting beaten like a rented mule.  And, he held on to this pass, where his helmet strap was permanently implanted in his cerebellum.

Fortunately, Gregg redeemed himself when he sent along this article to me for blog material: Obese Have Right to 2 Airline Seats Apparently, if you're "functionally disabled by obesity," you can get two airline seats for the price of one.  Yes, you read that right: being heftier affords you extra luxuries (most notably, avoiding the possibility of ever having to sit next to another obese person, which is something that I think would convince anyone to lose weight). It will be interesting to see if they go by Body Mass Index (BMI), which will probably rank every individuals who is actually dedicated to lifting weights as obese.  At 5-8. 190-195, I am literally on the border between "overweight" and "obese."  Forget First Class; I'm flying Fat A**! Kidding aside (okay, not really; I'm never serious), this opens us up to a lot of dangerous precedents that could be the fallout from this court ruling: 1. Smelly people get two deodorants for the price of one. 2. Folks who are seven feet tall get to go on the amusement park rides twice because they're twice as tall as the minimum height. 3. People who are soft tissue nightmares get two massages for the price of one (as if massage therapists aren't burning out too fast already) This list could go on and on.  Dangerous precedent, indeed. Thanks for the link, Gregg.  Sorry I had to inflict such violent fantasy football dominance on you.
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Warpspeed Fat Loss

In my newsletter earlier this week, I introduced you to Danny, a Cressey Performance client who had made some awesome progress on the Warpspeed Fat Loss diet over the course of 28 days. In reality, though, there’s quite a bit more to that story. You see, Danny had actually made a lot more progress than that since December of 2007 when he really committed to kicking a** and taking names. As was the case on Monday, a picture is worth a thousand words; here are the ten-month progress pictures:

In my last newsletter, I told you that this wasn’t just about “Hooray for Danny” or “Horray for Warpspeed Fat Loss” – although both definitely deserve all the credit in the world! Rather, I’m a firm believer that anytime someone is successful, you have to look at what they’ve done right – and these are the three things so important for Danny’s success.
1. Danny got involved with a great training crew. I don’t care who you are: a training crew will always yield better results. Danny actually lifts quite a bit with our staff nowadays. Hell, with all he’s learned, he’d be a great addition to our staff!
Obviously, I firmly believe that our job is to hammer on technique in a coaching-intensive set-up early on when someone trains at CP. However, I think that our longer-term responsibility is to create the most motivating environment possible in which to carry out our programming. Additionally, Danny had a great “crew” at home in the form of a very supportive wife who helped him on the diet side of things. It always helps to have someone along for the ride at home; I’ve seen a lot of people “sabotaged” by unsupportive family members. 2. Danny’s goal from the get-go was always performance. The physique stuff took care of itself when he just focused on getting stronger with each session and attended to his nutrition. Along the way, he got his first 300-pound bench and deadlifted well into the 400s. I have said it before and I’ll say it again: train for performance, put the right stuff in your mouth, and you’ll be pleasantly surprised at the physique improvements you see. It’s a theme that resounded in my Maximum Strength book. 3. Danny realized that you can always get a training effect in spite of injuries. When he first came to us, Danny had been dealing with some pretty significant neck spasms. In fact, when we went to work on some bench press technique the first night, he was pretty nervous that 95 pounds on the bar would trigger a spasm. Toss in a testy lower back, shoulder, hamstrings, and adductor strain, and you’d think that Danny would have been on the shelf for months. In reality, he didn’t miss a training session, as he appreciated that there was always something he could do to get better around those issues – and get better he did! These factors for success are just the tip of the iceberg, and they'll be different for everyone.  However, it's important to recognize them early-on and use them to your advantage, as getting leaner, stronger, faster, and healthier isn't always peaches and cream. The Truth About Unstable Surface Training: An Athletic Trainer's Perspective
“As someone who has both rehabbed injured athletes and trained healthy people for over 18 years, I can honestly say that Eric Cressey’s The Truth about Unstable Surface Training is a breath of fresh air."Being a certified athletic trainer and a strength and conditioning coach has afforded me a unique perspective in the training world. I have watched personal trainers, strength coaches, athletic trainers and physical therapists use and abuse unstable surface training. "Eric has combined his in-the-trenches experience with research to uncover the truth behind unstable surface training. This book is a must-read for anyone that trains, rehabs, or coaches, people in anyway. Yes, that means Physical Therapists, Athletic Trainers, Personal Trainers, and Strength Coaches. "I hope that this book will help to 'stop the madness' of a training fad that has gotten out of control and help to support the proper uses of unstable surface training. "I know I will be referring this work to my network of athletic trainers, strength coaches, physical therapists and personal trainers.” Keith Scott, MS, CSCS, ATC Certified Athletic Trainer, and Strength and Conditioning Coach www.BackToFormFitness.com
Click Here For More Information.
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Intermittent Fasting: Installment 2.0

Last week, I published a guest blog on the topic of intermittent fasting. Brad Pilon, Author of Eat Stop Eat, contacted me shortly thereafter with respect to the previous blog in question, and I encouraged him to pull together a submission of his own on the topic. I’m all for hearing all sides of every argument – and you can find Brad’s perspective below. I am largely known as the fasting guy, but what many people don’t know is that when I went back to school in 2006, I went back to “destroy” fasting. After seven years working in Research and Development for a sports supplement company, I was ready to go back to school to complete graduate studies in Nutritional Sciences. My plan was simple. I was going to spend a couple years studying all of the rules of nutrition, and then I was going to write my own nutrition book. After working in sports supplements for years, I thought I had a pretty good handle on exactly what I would find, the tricky part was figuring out where to start. After some thought, it became apparent to me that the obvious place to start my journey was to examine exactly what happens to the body in the absence of food – when we are fasting. Then, from there, I could start to investigate what happens when you eat different types of food. I was positive that the research would clearly show that after a couple of hours of not eating your metabolism would slow down. This isn’t what I found. Instead, study after study kept showing convincing evidence that even fasting for as long as 72 hours did not slow down your metabolism. This research was so convincing that I had no choice but to switch my plan and study the metabolic effects of short term fasting as the focus of my graduate work. So, I can completely understand why someone might be mislead to believe that fasting for a period of 12-72 hours could drastically suppressed their metabolism. After all, I thought this myself for a long period of time. However, once I became educated on the topic I realized that this belief is simply not supported by the available published research. So let’s take a look at the effect that fasting has on our metabolisms. When we say metabolism, or “thermogenesis,” we are really talking about the amount of calories we burn, typically in a 24-hour period. Obviously, from a weight loss perspective we want this to be as high as possible, and any evidence that would suggest a diet might lower our metabolisms is definitely not ideal. It has been a long held belief that our bodies quickly adapt to short periods of low calorie intake by lowering of our metabolism, but what does the research say? When I looked at the metabolic effects of short term fasting, I was shocked to find that even when a person does not eat for THREE DAYS, measures of metabolic rate either remain the same or actually increase during this short period of fasting. This has been found by a large group of papers, including those by Mansell in 1990, Klein in 1993, Carlson in 1994, Webber in 1994, Zauner in 2000, and most recently Gjedsted in 2007. In fact, the available body of research on short-term fasting is remarkably consistent in this finding: for both men and women, fasting for a period of 12-72 hours does not decrease metabolic rate. To examine this even further, we can take a closer look at the paper written by J. Webber and I.A. MacDonald, specifically because it has a large number of subjects, and it included both men and women. In this trial, all the people were studied on three different occasions after a 12, 36, or 72-hour fast. The studies were conducted in random order, and there was a gap of at least seven days of normal eating between each fast. Metabolic rate was calculated from a continuous recording of oxygen and carbon dioxide consumption and production, using a ventilated canopy (indirect calorimetry), which is a pretty standard measure of metabolic rate in research studies. The results of this trial showed that not only was there NOT a decrease in metabolic rate, but that there was actually a significant INCREASE in resting metabolic rate between 12 and 36 hours of fasting. We’re talking about roughly 100 calories, so nothing to get overly excited about, and I’m even willing to ignore this increase and say that while it was statistically significant, it’s probably not “real-world” significant. That being said, even when we ignore the increase in metabolic rate, we have to admit that there was definitely NO DECREASE in metabolic rate. So, in men and women who fast for as long as 72 hours long, there is NO decrease in metabolic rate. Based on this evidence, we can say that the practice of intermittent fasting (where a person fasts for 24 hours) will not decrease metabolic rate. There are other questions that need to be answered about the benefits of fasting, including how it affects fat burning, hormones like growth hormone, and muscle mass. For more information on the metabolic effects of short term fasting in humans, you can check out my book, Eat Stop Eat.
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I Am Laughing at this…

...but not for the reasons they'd like me to be laughing. Laugh Away Your Abs - Watch more free videos And, I don't feel any leaner.
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  • Avoid the most common deadlifting mistakes
  • 9 - minute instructional video
  • 3 part follow up series