Once the liver and muscles have reached their saturation points for glucose, excess glucose can be converted into fatty acids and stored as fat, for this to happen it needs to undergo the process of de novo lipogenesis (DNL) inside of the liver, this is where glucose, amino acids and alcohol can be converted into fatty acids (often short-chain fatty acids) which can travel through the bloodstream in the form of VLDL where it can then come in contact with the enzyme lipase which will release the fatty acids for storage inside of adipose tissue. The process of de novo lipogenesis (DNL) produces palmitate as a byproduct, which causes an increase in inflammation and has been linked to various diseases, this may advocate for a high-carb diet because this does not need to undergo this process to be stored as fat.

Insulin

The pancreas is made up of cells known as islets, there are beta cells which synthesise, store and release insulin and alpha cells which synthesise, store and release glucagon, which acts to break down glycogen into glucose. A normal blood sugar is 80-120 mg/dL, if an individual's blood sugar rises above this then insulin will be stimulated to be released, if an individual’s blood sugar drops below this then glucagon will be stimulated to be released.

When there is a high glucose concentration in the blood, glucose will diffuse into beta cells via glucose transporters. Glucose then enters the mitochondria and produces ATP, this means ADP is getting turned into ATP, so ADP is reduced in the cell and ATP is increased. ATP-sensitive potassium channels are located on the cell membrane and they remain open when ADP is bound to them this means that potassium will flow out of the cell, because potassium has a positive charge it means that the outside of the cell will become positive, whilst the inside of the cell will become negative. When ADP decreases in the cell due to the increase in glucose the ATP-sensitive potassium channels will no longer have any ADP bound to it and they will therefore close, and ATP will bind with it to keep it shut, because of this potassium can’t leave the cell and inside the cell becomes more positively charged and outside the cell becomes less positively charged, this will cause calcium channels in the cell membrane too open, calcium enters the cell and it stimulates vesicles filled with insulin to bind with the cell membrane releasing insulin into the bloodstream. These processes may not be allowed to happen if glucose can’t enter the cell, if there isn’t enough ATP, if calcium is not entering the cell, if potassium is not leaving the cell or if glucose can not be broken down in the cells for energy, due to a mutation in the glucokinase gene which means glucokinase can not be produced and turn glucose into glucose-6-phosphate, which will eventually help produce ATP. Problems which don’t allow insulin to be released from the pancreas are known as type 1 diabetes, this means blood glucose remains elevated in the blood which can damage blood vessels and lead to many problems, the most common cause of type 1 diabetes is due to an autoimmune disease which occurs when the body's immune system begins killing beta cells, creating an insulin resistance. Oral hypoglycemic agents known as sulfonylureas will close the  ATP-sensitive potassium channels this means potassium rises in the cell eventually leading to a release of insulin into the bloodstream. Glucose isn’t the only nutrient which can stimulate the release of insulin, amino acids, fatty acids and ketones can all jump into the process of the metabolism forming ATP from ADP which will lead to an insulin release, although not as much as glucose. Amino acids, fatty acids and ketones will stimulate a much greater release of insulin when combined with glucose than if they were on their own. Certain amino acids have a positive charge and some amino acids will enter the cell with sodium, which has a positive charge this will depolarise the cell when they enter it in a similar way to what potassium does this will lead to an insulin release. The parasympathetic nervous system is stimulated when you eat, relax or during mild exercise and it sends a signal down to the pancreas via the vagus nerve releasing acetylcholine which activates certain receptors in beta cells leading to an insulin release. The sympathetic nervous system is stimulated during danger or stress and it sends a signal to the adrenal glands via the preganglionic neurons which stimulates the release of cortisol and adrenaline, cortisol stimulates the breakdown of glycogen to glucose and adrenaline also will stimulate the breakdown of glycogen into glucose, but not too as large of a degree as cortisol, and it will also activate certain receptors in beta cells leading to an insulin release. Chronically elevated levels of cortisol will lead to chronically elevated levels of blood glucose which will bring about the negative side effects associated with this. There are types of digestive hormones released known as incretins which also stimulate the release of insulin. Somatostatin is released from the gastrointestinal tract, pancreas, hypothalamus, and central nervous system when glucose, fatty acids or amino acids are consumed, when glucagon levels rise in the blood or by the sympathetic nervous system during danger or stressful situations and it works to inhibit the release of insulin.
 

Insulin in the bloodstream will bind to receptors on the membrane of cells, this will activate a protein on the inside of the cell which travels over to glut-4 proteins and stimulates them to move to the membrane of the cell, they then imbed themselves in the membrane so glucose can pass through them and enter the cell. These are insulin-stimulated glut-4 proteins, but there are also exercise-induced glut-4 proteins, this is why exercise is an effective method for controlling blood sugar. Type 2 diabetes occurs when the receptors of cells stop reacting to insulin, causing insulin insensitivity, this means more insulin and glucose stay circulating around in the bloodstream. The glucose will travel to the kidneys where it can be secreted out of the body in what is known as glucosuria, this results in osmotic diuresis because the glucose will pull in water with it, the individual will start to urinate more often in what is known as polyuria as a result of this, this will cause a depletion in water and electrolytes leading to dehydration and/or a hyperosmolar state, which is when the body's organs are drained of water. The dehydration will stimulate the brain to drink more water, causing large amounts of thirst, which is known as polydipsia. The dehydration can also lead to renal failure in extreme cases due to the decreased blood flow travelling to the kidneys. Polyphagia is large amounts of hunger, this occurs in diabetics because insulin can not stimulate white fat cells to release leptin, which is the satiety hormone. Eventually, if the body is insensitive to insulin for long enough it will lead to beta cell atrophy which can cause even more problems. People with type 1 and type 2 diabetes inject themselves with insulin to combat the symptoms of diabetes.

The glycemic index (GI) is how much certain foods spike blood glucose. The glycemic index is calculated against a sugar drink, which is 50g of sugar dissolved in water, we can measure how much this spikes glucose, in mg/dl, and plot it on a line graph. 50g worth of digestible carbohydrate will be consumed in the form of food or drink and its effects on blood sugar is measured in mg/dl and plotted on a line graph. The area of the sugar drink on the graph and the area of the food or drink on the graph will be calculated. Divide the food or drink area by the sugar drink area and then multiply this number by 100 in order to get the results of a particular food or drink's glycemic index. A low GI score is under 55, a medium GI score is 55-70 and a high GI score is over 70. To determine a particular food or drinks GI score it must be tested on multiple participants on multiple different days. Many factors will affect how fast particular carbohydrates in food are digested, including their chemical structure, if the carbohydrates are refined, if the food or drink contains any other macronutrients, how much fibre is in the food or drink and its cooking method. Low GI foods include green vegetables and most fruits, medium GI foods include sweet corn, bananas and oat breakfast cereals, high GI foods include white bread, white rice, potatoes and sugary snacks. The glycemic index can be used to determine how much particular foods will stimulate insulin, this is useful as foods which cause a large rise in insulin will be more likely to create insulin resistance when consumed on a regular basis. Low GI foods are also more likely to keep you full for longer as glucose levels in the blood will be elevated over a longer period of time, whilst high GI foods create a large drop of glucose levels below baseline within just 2 hours after consuming them leaving you filling hungry. You may often hear the term simple and complex carbohydrates. Simple carbohydrates are monosaccharides, these don’t need to be broken down as much as other saccharides before entering the bloodstream, these foods typically are high on the glycemic index because they enter the bloodstream shortly after consuming them. Complex carbohydrates are disaccharides and polysaccharides these typically take longer to be broken down and enter the bloodstream than monosaccharides they are therefore lower on the glycemic index.

Glucagon

With low to normal amounts of blood glucose, only some glucose will enter alpha cells of the pancreas and produce ATP inside of the mitochondria, some of these will bind to potassium channels on the cell membrane which will partly close it and stop some of the potassium from exiting the cell, this will cause a slight depolarization of the cell, this slight depolarization in the cell means that calcium channels in the cell membrane will open and calcium will flow into the cell. Calcium will stimulate vesicles in the cell which are filled with glucagon to bind with the cell membrane and release glucagon into the bloodstream. If there are high amounts of glucose in the blood, large amounts of glucose will enter the alpha cells and produce large amounts of ATP which will bind to potassium channels closing them tightly so potassium quickly builds up in the cells, causing significant depolarization, this will cause the calcium channels to close so calcium can’t enter the cell and there is, therefore, no release of glucagon. Norepinephrine and epinephrine are parts of the sympathetic nervous system and they are believed to be able to directly stimulate glucagon synthesis and secretion, cholecystokinin and secretin are both hormones which are also believed to directly stimulate glucagon synthesis and secretion. Glucagon can break down glycogen to glucose in order to raise glucose levels, as I’ve previously mentioned, but glucagon can also bind to g protein-coupled receptors on the cells of adipose tissue which will activate GTP on the inside of the cell, this travels to and activates the effector enzymes adenylate cyclase, this then changes ATP into cyclic AMP (cAMP) which activates protein kinase A which activates the enzyme hormone-sensitive lipase which will break down triglycerides to glycerol and fatty acids which enter the bloodstream, the glycerol can travel to the liver where the enzyme protein kinase A will convert the glycerol into glucose and odd chain fatty acids, which can also be converted into glucose in the liver. Protein kinase A can also convert amino acids into glucose in the liver. The process of amino acids, glycerol and odd-chain fatty acids forming glucose is known as gluconeogenesis. Glucagon can also bind to g protein-coupled receptors on the cells of myocardial tissue which will activate GTP on the inside of the cell, this travels to and activates the effector enzymes adenylate cyclase, which then changes ATP into cAMP which activates protein kinase A which opens calcium channels in the cell membrane so calcium will enter the cell causing the contraction of the muscle, this will, therefore, increase an individuals stroke volume, cardiac output and blood pressure. Epinephrine is a hormone which has almost the exact same effects on the body as glucagon.

Carbohydrates digestion 

The digestion of carbohydrates begins in the mouth as our jaw, teeth and tongue begin to break down our food. Our salivary glands also begin to secrete saliva containing amylase which begins to break down the bonds holding the saccharides together. When the saccharides travel down to the stomach the amylase will become inactivated due to its acidic environment, this means that no saccharide digestion occurs in the stomach and it is not broken down any further. The food which has entered your stomach will then leave your stomach into the small intestine as a creamy paste called chyme. The pancreas will secrete amylase into the small intestine which will help to further break down saccharides. The cells of the intestines known as enterocytes contain brush border enzymes which are a type of enzyme which when secreted into the small intestine work to break down saccharides in different ways. Once the saccharides have been broken down into monosaccharides they can enter the enterocytes through sodium-glucose-linked transporters, two sodium ions will enter the enterocytes per one monosaccharide molecule. The monosaccharide can then enter the bloodstream via a glut-2 transporter. When sodium enters the enterocytes it draws water into the cell, sodium then enters the bloodstream in exchange for potassium via the sodium-potassium pump. As previously discussed not all saccharides can be broken down into monosaccharides to be absorbed into the bloodstream. These saccharides will move through the small intestines and eventually enter the colon of the large intestine, where it will encounter the colons bacteria and undergo fermentation, releasing byproducts, such as short-chain fatty acids, which can be used by the body or butyrate which can be used to feed the colon cells.

Sugar

Sugar is actually a disaccharide, made up of glucose and fructose. Fructose raises blood glucose levels more gradually than glucose when either of them is consumed alone, but when they are absorbed together fructose will enter the bloodstream much quicker causing a dramatic increase in blood sugar which will cause a dramatic insulin release increasing the chance of developing an insulin resistance and therefore type 2 diabetes. The monosaccharide galactose is much like glucose in how quickly it is digested.
 

When sugar enters the mouth and touches the outside of your teeth because it is so concentrated it has an osmotic effect and the fluid which fills the microtubules in the dentin of your teeth will flow out of your teeth, this flow of fluid will stimulate the nerves in your teeth causing pain for certain individuals, typically those with pre-existing tooth complications. Sugar can also react with plaque and make acidic byproducts which break down the enamel of your teeth, which could create cavities or a tooth abscess. 

Carbohydrate's effect on performance

Carbohydrates are not essential in the diet because glucose can be produced via gluconeogenesis in the body, however, it does make sense to consume carbohydrates to enhance athletic performance. Up to 80% of ATP production comes from glycolysis during medium rep range resistance training, this is the process of glucose being converted to pyruvate, but if glucose is not sufficient in the muscle cells then not enough ATP will be produced to cause the muscles to maximally contract and relying on gluconeogenesis to supply your body with the glucose it needs is likely inefficient. Glycogen is also often stored in close contact with key proteins involved in calcium release from the sarcoplasmic reticulum for muscular contraction, a lack of these glycogen stores is believed to cause a suboptimal environment for muscular contraction. A lack of glycogen in muscle cells has been proven to significantly impeded the number of repetitions an individual can do of an exercise, particularly for exercises in the high rep range, it is therefore very rarely a good idea for any individual to perform a low carbohydrate diet if they have aims for increasing muscle mass or strength. Even though carbohydrates are essential for maximal performance there is evidence that a low-carbohydrate diet and a high-carbohydrate diet have the same effect on anaerobic performance, all that matters is that carbohydrates consist of roughly 25% of total daily calorie intake. There is some evidence that those on a low-carbohydrate diet become what is termed keto-adapted and their body gets more use to fueling itself on a low-carbohydrate diet. Even though a low-carb diet has been shown to have no negative impact on an individual's anaerobic abilities it still may hinder an individual's ability to make improvements in strength or increase muscle mass over time, in fact in studies it has been proven that a low-carb diet combined with resistance training in previously untrained individuals will not cause any gains in muscle mass whilst the same training regime caused an increase in muscle mass for individuals consuming a regular amount of carbohydrates, however, it is important to bare in mind that the low-carb individuals were most likely in a calorie deficit, it has also been proven though in studies that a low-carb diet combined with resistance training in previously trained individuals has caused a loss in muscle mass whilst individuals who consumed a regular amount of carbohydrates and the same amount of protein per kilogram of body weight as the low-carb individuals saw an increase in muscle mass, however, it is important to bare in mind that the low-carb individuals were again most likely in a calorie deficit. The reason for low-carb individuals seeing suboptimal results for hypertrophy may be due to a low-carbohydrate diet's effects on intracellular signalling for muscle hypertrophy, AMPK in muscle cells may sense the lack of energy and look to conserve energy by inhibiting energy-consuming processes such as the activation of mTORC1, and it also will increase catabolic processes such as glycolysis, beta-oxidation and protein degradation, ketogenic diets have also been shown to impair mTOR signalling, p70s6k activation, translation and even decrease the number of genes which are responsible for muscle growth, also Akt phosphorylation is only significantly spiked in the presence of high glycogen stores, but there is also some evidence that glycogen levels have no effect on anabolic signalling. One thing that appears a certainty is that a low carbohydrate diet will decrease testosterone levels by roughly 100 ng/dL on average, which could host many negative health effects if this means that an individual's testosterone levels will fall under 300 ng/dL, these effects could include low sex drive, low sperm count, depression, sleep troubles and a loss in muscle mass. Cortisol levels have also been shown to rise in individuals who are consuming a low-carb diet, cortisol breaks glycogen down into glucose, which can lead to chronically elevated levels of blood glucose which can damage blood vessels and lead to insulin resistance.

Carbohydrate intake recommendations

For the reasons discussed in the last section, I would recommend consuming a minimum of 3g of carbohydrates per kg of body weight every day, and strength-based athletes should consume 4-7g of carbohydrates per kg of body weight every day, however, the amount of carbohydrates that you consume in a day depends on how many your body uses for fuel which can vary by as much as 4-fold between individuals at rest and during exercise, factors such as your exercise type, intensity and duration, your muscle fibre composition, diet, age, glycogen levels and genetics all will significantly affect how much carbohydrates your body needs to fuel itself. It has been hypothesised that consuming carbohydrates post-exercise will enhance the anabolic effects and therefore lead to more muscle growth over time. Carbohydrates alone are believed to enhance muscle growth but also the insulin response caused by consuming carbohydrates is believed to be necessary to cause an increase in muscle protein synthesis because low insulin levels have been proven to suppress muscle protein synthesis. Insulin is also believed to suppress catabolic processes but the method for this is not yet known, although it is believed to be at least partly due to the phosphorylation of PI3k/Akt which blunts certain catabolic processes. Due to insulin’s anticatabolic effects it would make sense to try to create a large spike in insulin levels shortly after resistance training when protein breakdown begins to rise and peak 3 hours after training. Ideally, the meal that you do consume after training will be the meal with the most carbohydrates in for the day because we do not want excessively high insulin levels by causing too frequent spikes of insulin, which will occur if you eat a high-carb meal after training and then another for your dinner. The impact of insulin on hypertrophy likely peaks at around 1500-3000 ng/dL which usually happens 1-2 hours after a mixed meal and stays elevated for 3-6 hours depending on the size of the meal, because these insulin levels remain elevated for so long, as long as a high carb meal is consumed close to training the effects of insulin on hypertrophy are likely maximised. Consuming a high-carb meal (1-1.5g of carbs per kg of lean mass) directly after exercise will significantly increase the rate of glycogen repletion, which is needed as exercise will significantly deplete glycogen stores by about 30% on average, glycogen will be particularly depleted in type 2 muscle fibres, delaying your carb intake by just 2 hours after training will decrease the rate of resynthesis by as much as 50%, this is due to an increase in exercise-induced glut-4 proteins and an increase in the activity of glycogen synthase, which is an enzyme responsible for glucose storage, however, glycogen will almost certainly be replenished within 24 hours after exercise in individuals who are no partaking in a keto diet, so consuming carbohydrates shortly after exercise to replenish glycogen levels will only really be necessary if you are planning on exercising more than once per day. It is important to note that just a 45g dose of whey isolate can also spike insulin to the 1500-3000 ng/dL range because amino acids are also highly insulinemic, so you can also rely on consuming a high protein meal before or after a workout to spike insulin, there is also evidence that the body becomes primed for anabolism following exercise by staying sensitive to nutrients and blunting muscle protein synthesis until protein is consumed. In terms of your source of carbohydrates, it should mostly come from low glycemic carb sources and you can argue that high glycemic carb sources before, during and after exercise will help to keep glucose levels topped up.