By Jeff S. Volek, Ph.D., R.D. ProSource
Carbohydrates are a staple in most people's diet, especially athletes. Official dietary guidelines encourage Americans to consume more than half their energy from carbohydrates. So carbs must be good for us right? After all, the government is a trustworthy source of information. You are probably thinking it depends on how much, what type, and when they are consumed. Yes these are all important variables to consider. But one often ignored fact is that people vary widely in their ability to metabolize dietary carbohydrate. This is important because identifying whether or not you are one of the people who struggle with dietary carbohydrate can help you choose a more effective diet to enhance health and performance.
What Does Carbohydrate Intolerant Mean?
Let's first go over a little physiology by reviewing what happens (or what should happen) when you consume a meal with carbohydrate. Most dietary carbohydrate is digested and absorbed as glucose. You only have about 1-2 teaspoons of glucose in your bloodstream and a typical meal may have 10 times that amount. Your body therefore has to process the incoming surge of glucose quickly by shuttling it into cells. If you are good at managing dietary carbs most of the glucose will be taken up by skeletal muscle. Once inside muscle the glucose is converted to glycogen, the storage form of carbohydrate in the body, or some of it is burned as fuel. This is considered a healthy disposal of carbs in someone who is carbohydrate tolerant.
In many people, however, a significant portion of blood glucose is diverted away from muscle and taken up instead by the liver where it is converted to fat. The metabolic term used to describe this process of turning carbohydrate into fat is de novo lipogenesis or DNL.
As you might guess DNL, shunting dietary carbs into fat, is not healthy. This is a form of carbohydrate intolerance. Over time, this stealth-like conversion of carbs to fat leads to increased levels of triglycerides (fat) in the blood, liver and other tissues and puts a person on the fast track to developing fatty liver, metabolic syndrome, and type 2 diabetes.
Insulin Resistance = Carbohydrate Intolerance
Rather than use the term carbohydrate intolerance, clinicians and researchers refer to the problem as insulin resistance. When you consume carbohydrate, blood glucose levels increase. In an effort to bring the blood glucose level back down to normal, your body releases the hormone insulin from the pancreas. Insulin opens the doors on muscle and other cells that allow glucose to enter. However, if you have insulin resistance, insulin only partially opens the door or in more advanced insulin resistance it may only crack the door open. This is because insulin resistance is a result of impaired insulin action in cells. Muscle is unresponsive to insulin. It's not doing its job efficiently. Thus, blood glucose gets backed up and the result is high levels of sugar in the blood. In the early stages of insulin resistance, the pancreas compensates by working harder to release greater amounts of insulin in response to consumption of carbohydrates. This may allow the doors on muscle cells to remain open, but it is at the expense of making the pancreas work harder by elevating insulin levels. High insulin has many drawbacks; in particular it significantly impairs your ability to burn body fat since insulin is a potent fat blocker.
Simply put if you have insulin resistance and you consume dietary carbohydrate, your body will struggle to metabolize it in muscle. Instead much of the blood glucose ends up getting processed in the liver where it is converted to fat. When viewed from this perspective, it is clear that insulin resistance, the hallmark of Type 2 diabetes, manifests functionally as carbohydrate intolerance.
A recently published study highlights this point. Lean insulin-resistant men were studied on two occasions after consumption of a high carbohydrate meal (1). On one occasion they remained sedentary throughout, and on the other they exercised for 45 min before consuming the meal. Detailed measures of how they processed the carbohydrate load were carried out for several hours after the meal. In the resting state, these insulin resistant men converted a significant amount of dietary carbohydrate to fat. However, when exercise was performed the conversion of carbohydrate to fat was reduced by 30% in the liver, and muscle glycogen synthesis was increased 3-fold. These results indicate that insulin resistance manifests as carbohydrate intolerance and that exercise can partially overcome the mismanagement of dietary carbohydrates by improving muscle insulin sensitivity.
A staggering 2 out of every 3 adults in the US are overweight and most of these people have some level of insulin resistance. One in three adults has metabolic syndrome, also called pre-diabetes, and about 1 in 4 have impaired fasting glucose. You don't have to be overweight to have insulin resistance, as was shown in the above study in normal-weight men (1). Some thin people, and even some high level athletes, have insulin resistance and signs of carbohydrate intolerance. Thus, carbohydrate intolerance is not a trivial problem. It affects tens of millions of people in the US. Even if you are carbohydrate tolerant now, it does not mean that will always be the case as aging is associated with insulin resistance.
How Do You Know if Your Body Is Metabolizing Carbs Efficiently?
This can be a little tricky because there is no easily performed perfect test to determine if you are carbohydrate intolerant. There are several clues that signal your body may be mismanaging dietary carbohydrates.
- Do you have a family history of diabetes? Insulin resistance is partially inherited so if other members of your family have it, you have a greater chance.
- Are you overweight? Being overweight is associated with insulin resistance.
- Do you carry extra fat in the mid-section? Central obesity (apple vs pear shape) is highly associated with insulin resistance.
- Do you bloat easily when you consume a lot of carbohydrates?
- Do you have trouble losing weight on a low fat/high carbohydrate diet?
- Do you lack energy and are unmotivated to exercise on a low fat/high carbohydrate diet?
- Do you have wide swings in energy throughout the day? This is a sign your blood glucose levels are unstable which occurs in people with insulin resistance.
- Do you get tired after consuming carbohydrate-rich meals? This is a sign you are over-stimulating insulin in response to being insulin resistant resulting in low blood sugar.
- Do you have strong cravings or intrusive thoughts for carbohydrate-rich foods?
- Do you have high levels of blood glucose (>100 mg/dL)
- Do you have high levels of blood triglycerides (>150 mg/dL)
What Can You Do About It?
If you have carbohydrate intolerance, there is a solution and hope. The answer may not surprise you. Similar to other food intolerances like lactose intolerance or gluten intolerance, the most logical approach is to limit the offending substance. In this case, restricting dietary carbohydrate to a level you can manage is priority number one.
Wait a minute you say -- athletes need carbs for energy, and having more glycogen, the storage form of carbohydrate in muscle, is tightly linked to performance -- right? The truth is it's not quite that straightforward. Trumpeting carbs as an ideal fuel source is often taught in academic institutions and reinforced by the billion dollar sports and energy drink market, but there is another perspective based on maximizing fat metabolism (more on this in future articles). For now let's continue the discussion of insulin resistance as it relates to glycogen.
Glycogen and Insulin Resistance (Carbohydrate Intolerance)
Glycogen, the storage form of carbohydrate in muscle, has garnered a special place in the hearts of exercise scientists and active individuals for over four decades. This began shortly after the advent of the biopsy needle in the mid 1960s, which allowed histological and biochemical studies of human muscle before, during and after exercise. Subsequent work detailing the importance of muscle glycogen as a fuel for active muscle during prolonged exercise, and the role of glycogen depletion with fatigue, dawned the age of high-carbohydrate diets as the optimal sports nutrition diet. Carbohydrate loading strategies were developed that super-saturate muscles glycogen levels, delay glycogen depletion, and prolong the onset of fatigue, thereby improving performance (2). Carbohydrate loading regimens have been modified (3) but remain popular today. This research led to the fundamental understanding of glycogen as purely an important energy substrate for contracting skeletal muscle.
The evidence showing that glycogen availability exerts a regulatory role on a range of metabolic processes has been less appreciated (4). In particular is the role of glycogen on insulin resistance and the cellular mechanisms that regulate transport of glucose into cells. As previously noted, insulin resistance is defined as a reduced ability of peripheral tissues to respond properly to insulin. In the case of skeletal muscle, there is a defect in insulin signaling that leads to decreased translocation of intracellular GLUT-4 to the plasma membrane and subsequent transport of glucose into the cell. Exercise has “insulin-like” effects in the sense that it causes an increase in glucose transport for some time after exercise. Although unclear, the signals that regulate glucose transport by exercise are different than those utilized by insulin (5).
Results from several experiments over the last two decades have shown that muscle glycogen levels exert an important influence on insulin-mediated and contraction (exercise)-mediated glucose uptake, as well as basal (unstimulated) glucose entry into cells. Glucose uptake is higher in glycogen-depleted muscle and there is an inverse relation between glycogen and glucose uptake across a broad range of glycogen levels (6,7). The majority of this work has utilized rats that are exercised to deplete muscle glycogen, and then fasted or fed diets of varying nutrient composition. At some time after exercise, muscles are dissected out or a surgical procedure is performed for isolated hindquarter perfusion followed by measurements of glucose transport activity and related metabolic and cellular regulators.
Numerous reports have confirmed that exercise induces an increase in skeletal muscle GLUT-4 and a proportional increase in glucose transport capacity. When carbohydrates are fed after exercise there is an increase glucose entry into cells that is diverted to glycogen formation. As glucose enters into cells and glycogen levels increase, there is inhibition of contraction- and insulin-mediated glucose transport that is associated with a return of GLUT-4 to pre-exercise levels. Notable, prevention of glycogen synthesis, by fasting or feeding a low-carbohydrate/high-fat diet, results in a persistence of an increase in contraction- and insulin-mediated glucose transport that lasts as long as long as carbohydrates are not consumed. Simply put, low glycogen promotes increased insulin action, whereas high glycogen promotes insulin resistance.
In one study, rats were exercised to deplete muscle glycogen and were then either fasted or provided with normal chow or a carbohydrate-free diet for up to 66 hr after exercise before being sacrificed (8). Active muscles were dissected for determination of insulin-stimulated glucose transport activity, glycogen, and GLUT-4 protein. Insulin-stimulated glucose transport and GLUT-4 protein were two-fold higher in muscles of exercised rats compared to sedentary animals. These effects were completely reversed in rats fed the high-carbohydrate diet after 42 hr, but in animals fed the carbohydrate-free diet the increased glucose transport and GLUT-4 persisted at 66 hr after exercise. These effects were closely tied to glycogen levels, which remained depleted in carbohydrate-free fed rats. The results indicate that prevention of glycogen synthesis after exercise results in a sustained increase in glucose transport capacity, presumably mediated by a prolongation of the exercise-induced increase in GLUT-4.
Similar experiments have shown that resting and contraction-mediated glucose transport capacity and cell surface GLUT-4 content 18-24 hr after exercise are significantly increased in rats fasted (9) or fed lard (7) versus a high-carbohydrate diet. These studies show the decreased contraction-mediated glucose transport capacity in glycogen-packed muscle cells is due to a proportionally smaller increase in GLUT-4 at the cell surface.
Although very low-carbohydrate studies in humans are few in the area of glucose metabolism, the existing data are mainly consistent with animal work. Insulin stimulates glucose uptake after exercise in relation to the amount of glycogen used (10). Low-carbohydrate diets are often likened to starvation in terms of lipid metabolism (11), but in respect to glucose metabolism there are distinct differences. In humans, starvation reduces insulin-mediated glucose uptake and does not increase nonoxidative glucose disposal (12), whereas very low-carbohydrate diets do not inhibit glucose uptake and augment nonoxidative glucose disposal (i.e., formation of glycogen) (13,14). Insulin-stimulated increases in glycogen synthase activity are greater after a very low-carbohydrate diet (14).
It seems obvious that the elegant work detailing the role of glycogen on metabolic and cellular control in muscle relating to glucose metabolism would have a place in determining and justifying nutritional guidelines, specifically for athletes, and individuals with glucose intolerance, insulin resistance, and Type II diabetes. Sadly, this has not been the case and it may be limiting your responsiveness to exercise.
Based on your genetics, you may have a certain level of insulin resistance (aka, carbohydrate intolerance). If you are over-consuming carbs and have a full glycogen tank, this may also elicit a form of carbohydrate intolerance. In either case, the logical solution would be to restrict carbohydrates which induce a partially glycogen reduced state (15) and widespread improvements in the way your body processes energy. The implications of your body composition, health and performance may be dramatic.
- Rabol R, Petersen KF, Dufour S, Flannery C, Shulman GI. Reversal of muscle insulin resistance with exercise reduces postprandial hepatic de novo lipogenesis in insulin resistant individuals. Proc Natl Acad Sci U S A. 2011 Aug 16;108(33):13705-9.
- Bergstrom J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol Scand. 1967 Oct-Nov;71(2):140-50.
- Sherman WM, Costill DL, Fink WJ, Miller JM. Effect of exercise-diet manipulation on muscle glycogen and its subsequent utilization during performance. Int J Sports Med. 1981 May;2(2):114-8.
- Hargreaves M. Muscle glycogen and metabolic regulation. Proc Nutr Soc. 2004 May;63(2):217-20.
- Richter EA, Derave W, Wojtaszewski JF. Glucose, exercise and insulin: emerging concepts. J Physiol. 2001 Sep 1;535(Pt 2):313-22.
- Hespel P, Richter EA. Glucose uptake and transport in contracting, perfused rat muscle with different pre-contraction glycogen concentrations. J Physiol. 1990 Aug;427:347-59.
- Derave W, Lund S, Holman GD, Wojtaszewski J, Pedersen O, Richter EA. Contraction-stimulated muscle glucose transport and GLUT-4 surface content are dependent on glycogen content. Am J Physiol. 1999 Dec;277(6 Pt 1):E1103-10.
- Garcia-Roves PM, Han DH, Song Z, Jones TE, Hucker KA, Holloszy JO. Prevention of glycogen supercompensation prolongs the increase in muscle GLUT4 after exercise. Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E729-36. Epub 2003 Jun 10.
- Kawanaka K, Nolte LA, Han DH, Hansen PA, Holloszy JO. Mechanisms underlying impaired GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats. Am J Physiol Endocrinol Metab. 2000 Dec;279(6):E1311-8.
- Richter EA, Derave W, Wojtaszewski JF. Glucose, exercise and insulin: emerging concepts. J Physiol. 2001 Sep 1;535(Pt 2):313-22.
- Klein S, Wolfe RR. Carbohydrate restriction regulates the adaptive response to fasting. Am J Physiol. 1992 May;262(5 Pt 1):E631-6.
- Mansell PI, Macdonald IA. The effect of starvation on insulin-induced glucose disposal and thermogenesis in humans. Metabolism. 1990 May;39(5):502-10.
- Bisschop PH, de Metz J, Ackermans MT, Endert E, Pijl H, Kuipers F, Meijer AJ, Sauerwein HP, Romijn JA. Dietary fat content alters insulin-mediated glucose metabolism in healthy men. Am J Clin Nutr. 2001 Mar;73(3):554-9.
- Cutler DL, Gray CG, Park SW, Hickman MG, Bell JM, Kolterman OG. Low-carbohydrate diet alters intracellular glucose metabolism but not overall glucose disposal in exercise-trained subjects. Metabolism. 1995 Oct;44(10):1264-70.
- Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism. 1983 Aug;32(8):769-76.