This is going to be a pretty long article, but it’s worth reading if you want to learn everything you need to know about carbohydrates, how body biochemistry works in order to digest and absorb them, how they impact fat loss, their effect on fat gain, their impact on insulin and blood sugar levels, as well as get an answer to the dreaded “is a carb a carb” question.
Since I’m going to get extremely technical I’ve added a tldr; section at the end of the article summarizing the main take home messages.
Table of Contents
- What Are Carbohydrates?
- Carbohydrates And Glycogen
- Glycogenesis And Glycogenolysis
- Glycogen And Exercise
What Are Carbohydrates?
Carbohydrates are the most abundant organic molecules on earth. They are the main structural component of plants and they provide food energy in the form of starch and sugars. In fact, carbohydrates provide more than half of the food energy consumed by humans worldwide. Carbohydrates also act as metabolic intermediates, as constituents of RNA and DNA, as structural elements of cells and tissues, as well as energy storage molecules in the body. The functional diversity of carbohydrates is due to their structural diversity.
Carbohydrates are constructed from carbon, oxygen, and hydrogen atoms that occur in a proportion that approximates that of a “hydrate of carbon,” (C‒H2O)n, accounting for the term carbohydrate. To be more precise, carbohydrates are aldehydes or ketones that have multiple hydroxyl groups.
Carbohydrates are usually categorized into simple carbohydrates and complex carbohydrates. Simple carbohydrates include monosaccharides and disaccharides. Monosaccharides are structurally the simplest form of carbohydrate in that they cannot be reduced in size to smaller carbohydrate units by hydrolysis. Examples of simple carbs include:
- glucose (dextrose)
- fructose (fruit sugar)
- lactose (milk sugar)
- maltose (hydrolyzed starch found in beer and malt beverages)
- sucrose (table sugar/cane sugar).
Complex carbohydrates include oligosaccharides (oligo meaning ‘few’) containing 3–10 saccharide units and polysaccharides (poly meaning ‘many’) containing more than 10 units.
- Oligosaccharides are found in beans, peas, bran and whole grains. These products often make you gassy, because the digestive enzymes cannot hydrolyze oligosaccharides: only the bacteria of the intestines can digest them.
- Polysaccharides include starch, with its 2 forms amylose and amylopectin (both polymers of glucose). Starch is found in potatoes, cereal grains, legumes, as well as other vegetables. Amylose contributes ~20% and amylopectin ~80% of the total starch content of these foods. Glycogen, which is the body’s stored form of glucose, is also a polysaccharide, as is cellulose.
Although it’s easy to classify simple carbs as “bad” and complex carbs as “good“, the distinction between simple and complex carbs is in fact completely arbitrary. It is merely a convention that we call carbohydrates with 3 or more sugars “complex carbs” and carbohydrates with 1 or 2 sugars “simple carbs”.
Does that also mean that a carb is a carb when it comes to fat loss? Are 50 grams of sugar more fattening than 50 grams of rice? Should you limit your fruit intake to avoid fructose overconsumption? It’s true, not all carbohydrates are created equal.
Let’s take sugar for example. Sugar is widely believed to be excessively fattening. Many believe that calorie per calorie, sugar is more fattening than other carbs. Others point out that all carbs end up as glucose in your body and therefore a calorie is a calorie.
Both arguments are often countered by theories involving insulin and that “a calorie is a calorie” doesn’t mean that all calorie sources have the same effect on your body composition. Foods differ in their effects on your metabolism and their ease of absorption, so what is the truth? You can’t simply take into account that since bodybuilders eat rice as their main carb source and they’re jacked while those that add sugar to their coffee are fat therefore rice is better than sugar.
The problem with most studies is that they don’t control the intake of other macronutrients, nor even protein or total caloric intake, and often use ad libitum (Latin for “as much as you want”) eating protocols.
With that being said, on an ad libitum setting, if you keep adding sugar to your coffee, protein shakes and/or oatmeal, the most likely scenario is for you to gain weight or lose less weight if you’re on a caloric deficit, because sugar has an extremely low effect on satiety (feeling full). Since sugar tends to make foods taste better, you end up eating more, increasing your caloric/energy intake in the process.
We know that the body follows the laws of physics, so taking into account the laws of thermodynamics, if you eat more calories than the amount you burn, then you will gain weight. Since excess energy can be stored as fat mass, that’s exactly why you often gain fat in an energy surplus. Likewise if you eat less you lose weight.
After taking all of the above into account, it becomes obvious that when assessing the effect different types of carbohydrates have on your physique, instead of focusing on studies following ad libitum protocols, we want to read studies that actually compare groups of people that are identical in all respects, except the source of the carbohydrates in their diets and then look if these different diets resulted in different body composition changes.
This study divided 390 participants into two groups for 6 months. The first group ate a diet high in complex carbs whereas the other group ate a diet high in simple carbs. Both diets contained the same amount of calories and carbohydrates in total, leading to no differences in fat loss or muscle retention, as well as having identical effects on blood lipids.
Other studies [1, 2] support the above findings that diets containing different amounts of sugar resulted in the same body composition changes. Similarly, another study replaced part of a diet’s complex carbs by simple carbs likewise did not result in any changes in body composition.
This systematic review of the literature on the effects of fructose on body weight, concluded that substituting fructose for other iso-caloric carbs does not cause weight gain. It’s a myth that fructose is more fattening than other carbs, when calories are equated, at least within practical settings when you’re not consuming well over a hundred grams of pure fructose.
When it comes to pure body composition or bodybuilding purposes, it doesn’t matter if the carbs in your diet come from simple or from complex sources, as long as the total amount is still the same.
Carbohydrate Absorption And Digestion
Before dietary carbohydrates can be used by the body’s cells, they must first be hydrolyzed into their constituent monosaccharides within the gastrointestinal (GI) tract. Only monosaccharides can be absorbed into intestinal mucosal cells (enterocytes). The hydrolytic enzymes involved in digestion of complex carbohydrates and disaccharides are called glycosidases or carbohydrases.
Glucose and fructose, when present in food as monosaccharides, require no digestion prior to being absorbed into intestinal
cells. Poly-, tri-, and disaccharides must be hydrolyzed first.
Digestion of the starches, amylose and amylopectin, starts in the mouth. The key enzyme is salivary a-amylase, a glycosidase that specifically hydrolyzes a(1-4) glycosidic linkages. a-Amylase is unable to hydrolyze the b(1-4) bonds of cellulose, the b(1-4) bonds of lactose, the a(1-2) bonds of sucrose, and the a(1-6) linkages that form branch points in amylopectin. Given the short period of time that food is in the mouth before being swallowed, this phase of digestion produces mostly oligosaccharides (dextrins), but few mono or
disaccharides. The salivary a-amylase action continues in the stomach until the gastric acid penetrates the food bolus and lowers the pH sufficiently to inactivate the enzyme.
The dextrins move into the duodenum and jejunum, where they are acted upon by pancreatic a-amylase. The presence of pancreatic bicarbonate in the duodenum elevates the pH to a level favorable for enzymatic function. Pancreatic a-amylase continues to hydrolyze a(1-4) glycosidic bonds to produce maltose, maltotriose, and limit dextrins. Maltotriose contains three glucose units with a(1-4) linkages. Limit dextrins are branched remnants of amylopectin containing the a(1-6) linkage that a-amylase is unable to hydrolyze.
The maltose, maltotriose, and limit dextrins are further digested by specific enzymes in the enterocyte brush border. Maltose and maltotriose are hydrolyzed by a-glucosidase (also called maltase). Limit dextrins are acted on by a-limit dextrinase (also called isomaltase). a-Dextrinase is the only intestinal enzyme that will hydrolyze a(1-6) glycosidic bonds. Ultimately, glucose is the final digestion product of the combined action of a-amylase and the brush border enzymes.
A portion of the starch of beans and certain vegetables and other resistant starches are not fully digested. This is partially due to the inaccessibility of the food to the enzyme and to naturally occurring inhibitors of a-amylase and a-glucosidase in some foods. The latter observation has led to the use of enzyme inhibitors to slow starch digestion for controlling glycemic response.
No significant digestion of disaccharides or small oligosaccharides occurs in the mouth, stomach, or lumen of the small intestine. Digestion of disaccharides takes place almost entirely within the brush border of the upper small intestine via disaccharidase activity. The resulting monosaccharides immediately enter the enterocytes with the aid of specific transporters. Among the enzymes located on the enterocytes are lactase, sucrase, a-glucosidase (maltase), and trehalase. Lactase catalyzes the cleavage of lactose to equimolar amounts of galactose and glucose. As was pointed out earlier, lactose has a b(1-4) glycosidic bond, and lactase is stereospecific for this b linkage.
Lactase activity is high in infants, but in most mammals, including humans, it decreases a few years after weaning. This diminishing activity can lead to lactose malabsorption and intolerance. The frequency of lactose intolerance in human populations varies widely depending on geography, race, and ethnicity.
Sucrase hydrolyzes sucrose to yield one glucose and one fructose unit. a-Glucosidase (maltase) hydrolyzes maltose to yield two glucose units. Trehalase hydrolyzes the a(1-1) glycosidic bond of trehalose to yield two molecules of glucose. The final products of carbohydrate digestion, monosaccharides, can now be absorbed by the intestinal mucosal cells.
Practically all absorbable dietary starches and disaccharides are ultimately hydrolyzed completely by specific glycosidases to their constituent monosaccharide units. Monosaccharides, together with small amounts of remaining disaccharides, can then be absorbed by the intestinal mucosal cells.
Intestinal Absorption of Glucose And Galactose
The villi and microvilli of the intestinal brush border present an enormous surface area for nutrient absorption to occur. The absorptive capacity of the human intestine has been estimated to be about 5,400 g/day for glucose and 4,800 g/day for fructose—a capacity that would never be reached in a normal diet. Digestion and absorption of carbohydrates are so efficient that, under normal conditions, nearly all monosaccharides are absorbed by the end of the jejunum. After carbohydrate digestion, glucose and galactose are transported into the enterocyte by the same mechanisms involving both active transport (SGLTs) and facilitated transport (GLUTs).
- The active transport mechanism for glucose and galactose absorption into enterocytes requires cellular energy as ATP and the involvement of specific receptor: the glucose- galactose receptor has been designated sodium-glucose transporter 1 SGLT1.
- At times of high glucose concentration in the intestinal mucosa, such as after a large carbohydrate meal, glucose is transported into the enterocyte by facilitated transporter type 2 (GLUT2). GLUT2 also transports glucose, galactose, and fructose out of the enterocyte. This is procedure is known as facilitated transport. GLUT2 is selectively present in the apical membrane of the enterocyte so that it reduces intestinal glucose absorption when blood glucose levels are high, keeping blood sugar levels stable. In insulin resistant individuals or those with type 2 diabetes, the receptor is resistant to the effect of insulin with the result that glucose continues to be absorbed at a higher rate and blood sugar levels rise excessively.
Intestinal Absorption of Fructose
Absorption of dietary fructose occurs by facilitated diffusion and is mediated primarily by GLUT5. GLUT5 has a high affinity for fructose and is not influenced by the presence of glucose. Fructose is not absorbed by SGLT1 and therefore its absorption does not require energy.
The rate of fructose absorption is much slower than that of both glucose and galactose but is increased when GLUT2 is present in the brush border membrane of the enterocyte, as discussed previously.
When the intracellular concentration increases, fructose is transported out of the enterocyte into the hepatic portal vein by GLUT2 in the basolateral membrane, the same transporter that moves glucose and galactose out of the cell. The facilitated transport process can proceed only down a concentration gradient, from the place where fructose concentration is high to the place where fructose concentration is low. At typical dietary intakes, there is no fructose beyond the portal vein. Fructose is efficiently absorbed by the liver, where it is phosphorylated (trapped essentially). Because fructose is absorbed entirely by facilitated diffusion, its overall absorption rate is slower than glucose or galactose, but faster than sugar alcohols such as sorbitol and xylitol, which are absorbed purely by passive diffusion.
Many individuals (about 60%) cannot completely absorb fructose when consumed in large amounts, ranging from 20 to 50 grams, resulting in water flowing into the intestine via osmosis. As a result of this malabsorption, they experience symptoms such as intestinal pain, gas, and diarrhea.
Following the intestinal absorption of glucose, galactose, and fructose, they enter the hepatic portal vein, where they are carried directly to the liver. Essentially all of the galactose and fructose is taken up by the liver through specific GLUTs and metabolized.
Both fructose and galactose can be converted to glucose derivatives and once fructose and galactose are converted to glucose derivatives, they, like glucose, can be stored as liver glycogen, returned to the bloodstream to maintain circulating glucose levels or catabolized for energy according to the liver’s energy demand. Little, if any, galactose and fructose are found in the peripheral blood, and these sugars are not directly subject to the strict hormonal regulation that is such an important part of glucose homeostasis.
Glucose is nutritionally the most abundant monosaccharide because it is the exclusive constituent of starch and also occurs in each of three major disaccharides. Like fructose and galactose, glucose is extensively metabolized in the liver, but its removal by that organ is not as complete as in the case of fructose and galactose. The remainder of the glucose passes into the systemic blood supply and is then distributed among other tissues, such as muscle, kidney, brain, and adipose tissue. Glucose enters the cells in these organs by facilitated transport. In skeletal muscle and adipose tissue the process is insulin dependent, whereas in the liver, kidney, brain and other tissues it is insulin independent.
Fructose sources like orange and pomegranate juice, offer large amounts of antioxidants and vitamins, as well as lower cholesterol levels, and decreased levels of liver enzymes and body mass index (BMI).
The Glycemic Index (GI), Blood Sugar Spikes And Crashes
Glucose is used by a wide variety of cell types that rely on its supply to form ATP and therefore generate energy to keep the cellular processes active. Under normal conditions glucose’s concentration in the blood must be precisely controlled to keep all bodily processes functioning smoothly. The symptoms associated with diabetes mellitus are a graphic example of the consequences of a disturbance in glucose homeostasis.
Although, like we explained above, practically all dietary carbohydrates will end up as glucose in the blood, different carb sources can affect the rate at which glucose appears in the blood.
The effect of food on your blood sugar is measured by the glycemic index (GI). It is widely said that table sugar causes a massive blood sugar spike followed by a complete crash due to its high glycaemic index. That is false.
The glycemic index (GI) is a ranking of carbohydrates on a scale from 0 to 100 according to the extent to which they raise blood sugar levels after eating. Foods with a high GI are those which are rapidly digested and absorbed and result in marked fluctuations in blood sugar levels. Low-GI foods, by virtue of their slow digestion and absorption, produce gradual rises in blood sugar and insulin levels. You’ll find significant variation in these values due to differences in methodology, as even the temperature of food impacts its GI.
A related quantitative measure, the glycemic load (GL), considers both the quantity and the quality of the carbohydrate in a food. The glycemic load equals the glycemic index times the grams of carbohydrate in a typical portion of the food.
Table sugar, due to its 50% fructose content, has a GI of ~68, which is a ‘medium’ effect on blood sugar. In fact, table sugar even has a lower GI than whole-wheat bread, which has a GI of ~72. The same thing applies to the insulin index.
The glycemic index of a diet does not determine its effects on body composition.
This study compared weight loss diets with the same energy content and macronutrient composition, but a different glycemic index (and therefore load), finding no changes in muscle retention or fat loss between groups. Markers of health were unaffected, including blood pressure, heart rate, fecal patterns, glucose and insulin metabolism as well as blood lipids. The only different effect between the groups was a greater decrease in LDL cholesterol in the low-glycaemic load group.
Similarly, these results were replicated in a study focused on weight gain instead of weight loss.
Maintaining normal blood glucose concentration is an important homeostatic function, requiring the coordinated effort of the small intestine, liver, kidneys, skeletal muscle and adipose tissue. Regulation is the net effect of the organs’ metabolic processes that remove glucose from or return glucose to the blood. These pathways, are hormonally influenced, primarily by the antagonistic pancreatic hormones insulin and glucagon and to a lesser extent by the glucocorticoid hormones of the adrenal cortex.
The rise in blood glucose following the ingestion of carbohydrate, for example, triggers the release of insulin while reducing the secretion of glucagon. As a side note, there are only around 4 total grams of glucose in your blood at any time point. Insulin is the main hormone that lowers blood glucose levels and is the primary anabolic hormone. Insulin stimulates the cellular uptake of glucose, amino acids, and lipid, leading to their conversion to storage forms in muscle and adipose tissue.
The storage form of glucose, glycogen, is synthesized through the process called glycogenesis. Glucagon, the primary catabolic hormone having opposite effects on insulin, increases the breakdown of liver glycogen by a process called glycogenolysis. Additional mechanisms to increase blood glucose levels include an increase in the secretion of glucocorticoid hormones, primarily cortisol. Glucocorticoids cause increased activity of hepatic gluconeogenesis.
Insulin and GLUT4 play extremely important roles in the uptake of glucose in muscle and adipose tissue, especially following a carbohydrate-rich meal. The sequence of events involving insulin and GLUT4 are critical to normalizing blood glucose and thus preventing hyperglycemia. When blood glucose levels raise after eating, insulin is released by the b-cells of the pancreas into the bloodstream by a process of exocytosis. The circulating insulin binds with specific insulin receptors on cell membranes of muscle and adipose tissue.
Insulin binding causes GLUT4 to translocate to the cell surface, where it can remove glucose from the blood. Insulin binding also results in other important cellular responses. GLUT4 is an insulin-responsive transporter that is synthesized on the ribosomes of the rough endoplasmic reticulum and then transferred to the Golgi apparatus, where it is packaged into GLUT4 storage vesicles (GSVs). Binding of insulin to its receptor causes the GSV to translocate to the cell membrane.
Studies show similar weight loss with widely varying levels of insulin and there is no evidence for high insulin causing weight gain. Weight gain and overeating causes high insulin, not the other way around.
To sum it all up, this meta-analysis and systematic review, found that the effects of the glycemic index on health markers are dependent on the health markers’ initial values. What this means is that if you’re initially unhealthy, low glycemic load diets are good for your health, but if you’re healthy there is no effect. Additionally, people who are better aerobically trained show a lower GI response than those who are less well trained.
This is a perfect example of the ceiling effect. If something isn’t broken, then you can’t fix it. So if you’re already healthy, eating “healthy foods” at some point stops making you healthier. If you’re lean, you watch your diet and you’re physically active, then it’s safe to say you belong in the healthy category and the glycemic load of your diet has no considerable effect on your health.
When it comes to endurance exercise performance, this study found that ingestion of foods of different glycemic index 30 min prior to (one hour cycling) exercise does not result in significant changes in exercise performance, β-endorphin levels as well as carbohydrate and fat oxidation during exercise. It’s also important to note, that muscle tissue can utilise fructose as an energy source via glycolysis and glycogenesis, just not as a primary fuel substrate.
From a body composition standpoint, if you’re healthy, it makes no difference whether you eat low glycemic or high glycemic carbs, as well as simple or complex carbs. Similarly the source of carbs is generally only relevant if you’re unhealthy. If you’re already healthy, it generally doesn’t matter. In sum, when it comes to fat loss, a carb is a carb.
Of course, different carb sources contain not only different macronutrients, but micronutrients and vitamins that should also be taken into account for overall health. I’m obviously not telling you to stick to tablespoons of sugar as your only carb source.
Carbohydrates And Thermic Effect Of Food (TEF)
Specific dynamic action (SDA), also known as thermic effect of food (TEF) or dietary induced thermogenesis (DIT), is the amount of energy expenditure above the basal metabolic rate due to the cost of processing food for use and storage. Heat production by brown adipose tissue which is activated after consumption of a meal is an additional component of dietary induced thermogenesis. The thermic effect of food is one of the components of metabolism along with resting metabolic rate and the exercise component. A commonly used estimate of the thermic effect of food is about 10% of one’s caloric intake, though the effect varies substantially for different food components.
The thermic effect of food is the energy required for digestion, absorption, and disposal of ingested nutrients:
Carbohydrates And Fat Oxidation
Carbohydrates are rarely converted to fat, via a process called de novo lipogenesis, under normal dietary conditions. There are exceptions when this occurs. One is with massive chronic overfeeding of carbs, usually over 700-900 grams per day, for multiple days. Under those conditions, carbs max out glycogen stores, are in excess of total daily energy requirements and you see the conversion of carbohydrate to fat for storage. This however, is not a normal dietary situation for most people.
But by and large the conversion of carbohydrates to fat for storage is not a major pathway in humans. Of course, this doesn’t mean that carbohydrates can’t contribute to fat gain. When you eat more carbohydrates then you burn more carbohydrates and less fat. If fat burning is decreased, more of the fat that you are eating can then be stored as fat. So the effect is indirect.
Carbs don’t make you fat via direct conversion and storage to fat; but excess carbs can still make you fat by blunting out the normal daily fat oxidation so that all of the fat you’re eating is stored. Which is why a 500 cal surplus of fat and a 500 cal surplus of carbs can both make you fat.
They just do it for different reasons through different mechanisms. The 500 calories of excess fat is simply stored. The excess 500 calories of carbs ensure that all the fat you’re eating is stored because carb oxidation goes up and fat oxidation goes down.
Excess dietary carbs increases carb oxidation, impairing fat oxidation so more of your daily fat intake is stored as fat.
If you eat more carbs, you burn more carbs and burn less fat. If you eat less carbs, then you burn less carbs and burn more fat.
This doesn’t mean that low carb diets are superior for fat loss.
There is an abundance of research showing that fat loss is not affected by the ratio of carbohydrates to fat in the diet [1, 2, 3, 4, 5, 6], at least for sedentary individuals in non-ketogenic conditions and provided that protein and caloric intake are the same.
Carbohydrates And Glycogen
Glycogen is the major form of stored carbohydrate in animal tissues, located primarily in the liver (~100 g) and in skeletal muscle (~300-500 g normally). The glucose residues within glycogen serve as a readily available source of glucose. When dictated by the body’s energy demands, glucose residues are sequentially removed enzymatically from the glycogen chains and enter energy-releasing pathways of metabolism: glycogenolysis.
The cellular uptake of glucose requires that it cross the plasma membrane of the cell. The highly polar glucose molecule cannot move across the cellular membrane by simple diffusion because it cannot pass through the non-polar matrix of the lipid bilayer. In certain absorptive cells, such as epithelial cells of the small intestine and renal tubule, glucose crosses the plasma membrane (actively) against a concentration gradient, pumped by an Na+/K+- ATPase symport system (SGLT1).
Glucose is admitted to nearly all cells in the body by a carrier-mediated transport mechanism that does not require energy. A large number of transport proteins in the body facilitate the movement of specific substrates across cellular membranes into specific cells. The family of protein carriers involved in the transport of glucose is called glucose transporters, abbreviated GLUT. Different tissues use different GLUTs. The GLUT4 that transports glucose into muscle and adipose tissue is stimulated by insulin. Insulin translocates the preformed GLUT4 from intracellular vesicles to the cell membrane. In short, insulin is required for glucose to be rapidly transported into muscle cells.
Glycogenesis And Glycogenolysis
The term glycogenesis refers to the pathway by which glucose ultimately is converted into its storage form: glycogen. This process is vital to ensuring a reserve of quick energy.
This pathway is particularly important in hepatocytes (liver cells) because the liver is a major site of glycogen synthesis and storage. Liver glycogen can be broken down to glucose and reenter the bloodstream, playing an important role in maintaining blood glucose homeostasis. The liver can both produce glucose as well as reduce the blood glucose level when it becomes high and the liver is not dependent upon insulin for glucose transport into the cell, though glucokinase (enzyme that phosphorylates glucose) is inducible by insulin.
The other major site of glycogen storage is skeletal muscle. In human skeletal muscle, glycogen generally accounts for a little less than 1% of the weight of the tissue. Although the concentration of glycogen in the liver is greater, muscle stores account for most of the body’s glycogen (∼75%) because the muscle makes up a much greater portion of the body’s weight than the liver does. The glycogen stores in muscle are an energy source within that muscle fiber and cannot directly contribute to blood glucose levels, since muscle lacks the enzyme that converts the phosphorylated glucose back to free glucose.
The breakdown of glycogen into individual glucose units, in the form of glucose-1-phosphate, is called glycogenolysis and is catalyzed by the enzyme phosphorylase. Just like glycogenesis, glycogenolysis is highly regulated. The regulation is different for the phosphorylation isozymes in muscle than in liver, since the muscle and liver isozymes fulfill different physiological purposes.
- In muscle, the glucose is released from glycogen to provide glucose for energy within the cell.
- In the liver, glucose is released to provide blood glucose.
As phosphorylase (the catalyzing enzyme) is activated for glycogen phosphorylation, glycogen synthetase is inhibited.That means that the enzymes for glycogen synthesis and breakdown cannot be active at the same time.
Insulin is required for glucose to be transported into muscle cells, therefore making insulin production an important factor for maximum glycogen synthesis and muscle energy storage in order to be used during workouts. Since carbohydrate consumption stimulates insulin production, it has been theorized that you need to consume a lot of carbohydrates post-workout to help rebuild your glycogen stores.
Glycogen And Exercise
Even if a significant amount of glycogen is depleted, the body is very good at rapidly replenishing the fuel stores. Exercise causes translocation of GLUT4 from the GSVs to the cell membrane in your muscles to promote glucose uptake[1, 2], just like the effect of insulin.
This study, found that after performing sets of 6 leg extensions at 70% 1 RM until absolute failure occurred and not consuming anything afterwards, 75% of glycogen was restored after 6 hours. Is the “exercise” protocol used in the body weird? Absolutely, but it shows us how efficient the body at rapidly replenishing the fuel stores.
Depletion of muscle glycogen during exercise activates glycogen synthase, and this activation is greater when muscle glycogen is lower, resulting in a faster rate of glycogen resynthesis in the early post-exercise period. Following the cessation of exercise and with adequate carbohydrate consumption, muscle glycogen is rapidly resynthesised to near pre-exercise levels within 24 hours.
When rapid recovery of endogenous glycogen stores is a priority, ingesting glucose-fructose mixtures (or sucrose) at a rate of of ≥1.2 g carbohydrate per kg body mass per hour, can enhance glycogen repletion rates whilst also minimising gastrointestinal distress.
Keep in mind that most studies about glycogen depletion are performed on endurance athletes.
For the average Joe that barely lifts weights 3-4 times per week full glycogen storage depletion will most likely never occur.
If you’re an athlete training multiple times per week however, proper nutrition is of extreme importance.
Carbohydrates And Leptin
Leptin is a hormone predominantly made by adipose cells and enterocytes in the small intestine that helps to regulate energy balance by inhibiting hunger, which in turn diminishes fat storage in adipocytes. Leptin acts on cell receptors in the arcuate and ventromedial nuclei, as well as other parts of the hypothalamus and dopaminergic neurons of the ventral tegmental area, consequently mediating feeding. In obesity, a decreased sensitivity to leptin occurs (similar to insulin resistance in type 2 diabetes), resulting in an inability to detect satiety despite high energy stores and high levels of leptin.
Leptin is controlled primarily by:
- Acute energy balance in the short term. A high calorie deficit causes leptin to drop lower than what can be explained by fat loss, and a caloric surplus raises leptin higher than what can be explained by fat gain.
- Total amount of fat mass in the long term. Fat cells are factories for leptin production. Not having many factories obviously impairs production and the aboslute amount of leptin in circulation.
Regular carb refeeds acutely increase leptin, while fat has no effect, proving it beneficial to circulating leptin levels during the diet.
Tldr; To summarize all the above, regardless if the carbs you eat come from “healthy complex carbohydrates” or from cane sugar (glucose), both will inevitably end up as glucose just the same before they reach your blood stream. This is why from a fat loss standpoint, calorie per calorie, a carb is a carb, and starches and sugars are equally “fattening”.
You don’t need to worry about the glycemic index if you’re healthy. It is only when you’re not healthy and these homeostatic mechanisms do not function properly, that the GI of your food becomes relevant. Low glycemic load diets are good for your health if you’re initially unhealthy (like obese or diabetic), but in healthy populations there was no effect.
When it comes to body composition or for bodybuilding purposes, it doesn’t matter if the carbs in your diet come from simple or from complex sources, as long as the total amount is still the same.This doesn’t mean that you should completely avoid “healthier” low glycemic options. Different carb sources contain not only different macronutrients, but micronutrients and vitamins that should also be taken into account for overall health. Do not solely stick to tablespoons of sugar or candy as your only carb source. A balanced diet is best for overall health and adherence.
Fructose is absolutely fine for consumption, and when combined with glucose will replenish glycogen storage levels at a very rapid pace post workout. Fructose sources like orange and pomegranate juice, offer large amounts of antioxidants and vitamins, as well as lower cholesterol levels, and decreased levels of liver enzymes and body mass index (BMI). Fruit intake is also associated with lower levels of liver fat, heart disease, cancer and mortality.
Carbohydrates are rarely converted to fat, via a process called de novo lipogenesis, under normal dietary conditions. Carbs don’t make you fat via direct conversion and storage to fat; but excess carbs can still make you fat by blunting out the normal daily fat oxidation so that all of the fat you’re eating is stored. Excess dietary carbs increases carb oxidation, impairing fat oxidation so more of your daily fat intake is stored as fat.
Insulin is required for glucose to be rapidly transported into muscle cells.
For the average Joe that barely lifts weights 3-4 times per week full glycogen storage depletion will most likely never occur. If you’re an athlete training multiple times per week however, proper nutrition is of extreme importance.
Leptin is a hormone that helps to regulate energy balance by inhibiting hunger, which in turn diminishes fat storage in adipocytes. Regular carb refeeds acutely increase leptin, while fat has no effect, proving it beneficial to circulating leptin levels during the diet.