Home Posts tagged "Insulin"

Building Vibrant Health: Part 2

This post is a continuation of a guest submission from Eric Talmant.  In case you missed it, be sure to check out Part 1. No two people are alike.  Enter Metabolic Typing®, or what I like to call common sense.  In the 1930s, Weston Price discovered, by visiting many parts of the world, that there was a link between modern eating habits and the degree of chronic degenerative illness.  He also concluded that there was no such thing as a uniform, "healthy" diet (1).  Due to a myriad of variables including climate, environmental conditions, common food supplies, etc., different cultural and ethnic groups have developed different kinds of dietary requirements. Over the years, Price's initial research began to demonstrate more and more clues as to the optimal way to eat for improved health and well-being.  In the late 70s and early 80s, William Wolcott made a revolutionary discovery by proving that the body's Autonomic Nervous System and the oxidative system were connected.  This discovery allowed Wolcott to very accurately predict what kinds of foods each person needs to establish a balance between these two aforementioned systems.  Once given the proper nutrients, Wolcott was able to show the body's true capacity to regulate and heal itself. It is all about balancing body chemistry, which is unique for each one of us.  We all process foods and utilize nutrients differently. It is these differing genetic requirements that explain why broccoli may be fine for some of you, not affect some of you, and cause some of you to feel not so good (1).

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In the "average" person, every cell in the body is designed to be healthy and effectively carry out its specific job.  If our cells are not given the proper nutrients, they can lose the ability to do their specific job, which results in a low production of energy.  They also lose the ability to repair and rebuild tissue. Powerlifters and athletes would read this as the ability to recover from training.  Sickly ones replace healthy cells, which begins a cascading effect upon your entire body.  The worst case scenario is that the cells of an organ become so weak that the organ itself becomes inefficient. A good example is the pancreas and its ability to produce insulin.  We learned that the more insulin resistant a person becomes, the more insulin the pancreas must produce in order to carry out its functions.  Eventually the pancreas will not produce enough insulin and the result is that some type 2 diabetics end up having to inject insulin.  Therefore, rather than focusing on debating macronutrient consumption (protein, carbs, and fats), we will first identify our unique body's proper nutrients.

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In order to identify these nutrients that our bodies have a genetic need for, we need to first figure out what our needs are.  This is the main reason behind figuring out your Metabolic Type. Remember in the last article when I mentioned the shortcomings of treating insulin, high blood pressure, and cholesterol?  We always want to treat the underlying causes, not the symptoms.  Stress, illness, lack of endurance in the gym, inability to put on muscle mass or get stronger, high body fat, etc. are all symptoms.  What we eat, however, is one of the causes. Our dietary needs are very much determined by heredity.  As previously mentioned, various cultures have developed distinct nutritional needs as a result of elements such as climate, geographic location, and what types of edible plants and animals their environments had to offer.  For example, many of the indigenous people who live at or near the equator have a strong hereditary need for diets high in carbohydrates i.e. fruits, vegetables, grains, and legumes.  In contrast, the ancestral diets of Eskimos consisted primarily of protein and fat in order to keep warm and allow them to survive.

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Enter the United States, where we are a melting pot of many different ethnic and cultural backgrounds.  Simply put, because of the endless combinations it is just not possible for most of us to accurately identify what our ancestral diet might be; not to mention that our nutritional requirements are also determined by our lifestyle, environment, activity level, body composition goals, etc.  Although important, there are many other factors that identify our nutritional needs.  Enter the science of Metabolic Typing®. Remember the breakthrough that Wolcott discovered between the Autonomic Nervous System and the oxidative system that was mentioned in the opening paragraph?  The Autonomic Nervous System (ANS) controls all involuntary activities of the body.  Immune activity, breathing, heart rate, digestion, body repair and rebuilding, etc. are just a few of the many functions.

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It is our auto-pilot system because it keeps us alive without our conscious efforts or participation.  As such, it is often referred to as the "master regulator of metabolism". There are two opposing but complimentary branches that make up the ANS, the sympathetic branch and the parasympathetic branch; yin and yang if you will.  The sympathetic system controls those bodily functions that pertain to energy utilization such as the adrenals, thyroid, and pituitary.  Thus, it is known as the "fight or flight" branch. For example, when Togo the Caveman is suddenly startled by a T-Rex (or a mugger, as the contemporary case may be), his sympathetic system immediately stops digestion, gets blood out to the muscles, and speeds up his heart rate.  The parasympathetic system controls those bodily activities that relate to energy conservation such as repairing and rebuilding, digestion, waste elimination, etc.  It is known as the "rest and digest" branch. In most people, one branch has stronger neurological influences over the other, which results in a metabolic imbalance.  If the imbalance becomes too great, it has been discovered that diseases are more prone to develop.  Conversely, if the ANS is in balance (or close to) then health is more prone to be vibrant. Researchers Francis Pottenger and Royal Lee discovered that people have many different physical, psychological, and behavioral characteristics that match up with either sympathetic or parasympathetic dominance.  In addition, certain foods and nutrients have the ability to strengthen whichever side of the ANS is weaker (Wolcott's aforementioned colossal discovery), but I am getting ahead of myself.  Therefore, with the help of all these factors, Metabolic Typing enables us to identify which system is more dominant and then recommend those foods that will be more likely to establish balance.  Since the ANS is the master regulator of metabolism, proper food recommendation is very important. This is pretty cool, huh (1)? While the ANS is concerned with the upkeep and regulation of energy, the oxidative system addresses the rate at which food and nutrients are converted to energy within the body.  It involves three important processes: Glycolysis, Beta Oxidation, and Citric Acid Cycle/Krebs Cycle.

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Roughly one-fifth of the energy created from our food comes from the oxidation of carbohydrates in a process known as glycolysis.  Glycolysis is the metabolic breakdown of glucose and other sugars that release energy in the form of ATP (Adenosine triphosphate).  The other four-fifths come from the Citric Acid Cycle or Krebs Cycle.  Simply put, energy is produced in the Krebs Cycle from a combination of the right amount of oxaloacetate (from the oxidation of carbohydrates in glycolysis) and the right amount of acetyl coenzyme-A (from the metabolism of fats in a process known as Beta-Oxidation).  The glycolysis simply concerns the metabolism of carbohydrates.  Beta-oxidation is involved in fat metabolism.  These two components produce energy in the Krebs Cycle, and they are needed in the right amounts.  If there is too much oxaloacetate and not enough acetyl coenzyme-A, or vice versa, then energy production will be lacking.  This determination of how our bodies execute energy production is known as cellular oxidation. (1) In 1981, George Watson published Nutrition and Your Mind. After extensive study, he came to the conclusion that biochemical imbalances were at the root of many psychological problems.  He accidentally discovered that certain foods and nutrients increased adverse emotional states in some people, while the same foods and nutrients could lessen emotional problems in others.  Again, different people required different foods to promote health and wellness.  Instead of using the ANS as the basis for classification, he used cellular oxidation.  (Now that we know what it is and how it works, we can follow Watson's process.)  He conclusively discovered that there is a direct and profound correlation between a person's emotional and psychological characteristics and the rate at which their cells convert food into energy. He observed that some people burned food too slowly, while others burned it too quickly.  More importantly, this rate of cellular oxidation, which is determined by heredity and environmental influences, can be significantly altered by diet.  Here was another piece of the puzzle in balancing body chemistry, which is conducive to optimum health and wellness.  Now we need to figure out whether you are a slow oxidizer, a fast oxidizer, or a mixed oxidizer by determining which characteristics (individual to you) apply to each. (1). Fast oxidizers depend too much on the oxidation of carbohydrates in glycolysis for energy production.  They have a tendency to burn carbohydrates too quickly, which results in an excess production of oxaloacetate (explained above).  Obviously, a high carbohydrate diet will only make the problem worse.  However, since proteins and fats are dietary sources of Acetyl Co-A, which is lacking, they will help stimulate and sustain beta-oxidation, which is needed.  This will help balance the body chemistry and stabilize energy production. (1) Similar to fast oxidizers, slow oxidizers have the same problems with energy production but for the opposite reasons.  They are poor at carbohydrate oxidation in glycolysis and thus are inclined to be lacking in the production of oxaloacetate.  In their case, a higher carbohydrate diet will benefit the slow oxidizers by giving them dietary sources for oxaloacetate.  Since they also require lower amounts of Acetyl Co-A to balance their body chemistry, as well as different nutrients to stimulate and sustain glycolysis, slow oxidizers benefit from a diet that involves less protein and fat than the fast oxidizer. (1) Each oxidizer requires different types of foods and different mixes of those foods in order to optimally and efficiently convert nutrient into energy.  With sufficient available energy, your body's cells can properly carry out their genetic roles of repairing and reproducing maximally.  For example, let's say that you are a slow oxidizer but you are not eating sufficient amounts of carbohydrates.  Some of your food will not be converted to energy and will become prone to being stored as fat.  You will probably experience fatigue and hunger following meals, as well as indigestion and a lack of stamina.  Finally, your body's immune system will become weakened and you will be susceptible to colds and infections.  Being sick is certainly not my cup of tea. Mixed oxidizers are not that complicated.  Because of their "balanced" oxidative systems, proper energy production comes from relatively "equal" amounts of protein, carbohydrates, and fats. Each oxidizer requires different types of foods and different mixes of those foods in order to optimally and efficiently convert nutrient into energy.  With sufficient available energy, your body's cells can properly carry out their genetic roles of repairing and reproducing maximally.  For example, let's say that you are a slow oxidizer but you are not eating sufficient amounts of carbohydrates.  Some of your food will not be converted to energy and will become prone to being stored as fat.  You will probably experience fatigue and hunger following meals, as well as indigestion and a lack of stamina.  Finally, your body's immune system will become weakened and you will be susceptible to colds and infections.  Being sick is certainly not my cup of tea.

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Now we understand the Autonomic Nervous System and the oxidative system.  These are the key homeostatic systems that determine our metabolism or our Metabolic Type®. However, the fun is just beginning!  We have defined these two big powerhouses that influence our metabolism, but how are we to know which system is more prevalent?  We will discuss system dominance and the actual Metabolic Types in the next article.  We will be discussing macronutrient ratios for each type, as well as some fascinating stuff on exactly how a single food can alkalinize the chemistry of one person, while acidify the body chemistry of another.  Finally, we will discuss which specific foods are optimum for each type and why.  Sit tight, as the rubber is about to meet the road... About the Author Eric Talmant is a top lightweight powerlifter and has a "passion for all things nutrition." A 1996 graduate of the University of Evansville, Eric is a certified Metabolic Typing® advisor http://www.mt-advisors.info/EditIndex.php and Functional Diagnostic nutritionist.  Talmant is certified to offer the Advanced Metabolic Typing® Test as well as order blood work (the Signet MRT Test,  U.S. BioTek ELISA IgG allergy test, the High Sensitivity C-Reactive Protein heart health test, and the BioHealth Diagnostics Adrenal and Hormone Profiles to name a few) and dispense hormones. Eric has competed in the ADFPA, NASA, AAPF, APF, APA, the WPO, and the Raw Unity Meet.  He holds the APF Florida state men's open equipped squat record of 678 pounds. He has been ranked in the top in the 75K class among all raw lifters in the United States for the past two years and he was a top equipped lifter in the two years before that. His best equipped lifts are a 683 pound squat, 391 pound bench press, and a 650 pound deadlift in the 75K weight class. His best raw lifts to date are 485 pound squat without knee wraps, 290 pound bench press, and 635 pound deadlift. He is also the founder and contest director of the Raw Unity Meet, which experienced great success in 2008 and 2009.  Talmant brings a unique skill set of 16 years of nutritional experience to his sponsors BMF Sports, Ultra Life, Inc., Critical Bench, and Titan Support Systems.  He lives in Spring Hill, FL and can be reached through EricTalmant.com.

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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.

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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. 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