The form of carbohydrates ingested before exercise may have different effects on both metabolism and performance. Moreover, the ingestion of solid foods slows gastric empty, digestion and absorption rates compared with liquid foods and this has a different impact on glycemia.
For these reasons, several studies have investigated the effects of the form of carbohydrates on glycemic responses, oxidation rates and performance.
Studies comparing solid versus liquid carbohydrates and solid versus gel carbohydrates have found no difference in glycemic responses between groups.
Studies that have investigated difference in performance effects have found no differences.
Furthermore, no differences are found in carbohydrate oxidation rates between the carbohydrate ingestion in the three forms during exercise.
Hypoglycemia: strategies to limit it in susceptible subjects
From several studies it appears that the risk of developing hypoglycemia (blood glucose < 3.5 mmol /l or < 63 mg/l) is highly individual: some athletes are very prone to develop it and others are much more resistant.
A strategy to minimize glycemic and insulinemic responses during exercise is to delay carbohydrate ingestion just prior to exercise: in the last 5-15 min before exercise or during warm-up (even though followed by a short break). Why?
Warm-up and then exercise increase catecholamine concentrations blunting insulin response.
Moreover, it has been shown that ingestion of carbohydrate-containing beverages during a warm-up (even if followed by a short break) does not lead to rebound hypoglycemia, independent of the amount of carbohydrates, but instead increases glycemia. When carbohydrates are ingested within 10 min before the onset of the exercise, exercise will start before the increase of insulin concentration.
Therefore, this timing strategy would provide carbohydrates minimizing the risk of a possible reactive hypoglycaemia.
In addition, it is possible to choose low glycemic index carbohydrates that lead to more stable glycemic and insulinemic responses during subsequent exercise.
An intriguing observation is the lack of a clear relation between hypoglycaemia and its symptoms (likely related to a reduced delivery of glucose to the brain). In fact, symptoms are often reported in the absence of true hypoglycemia and hypoglycemia is not always associated with symptoms. Though the cause of the symptoms is still unknown, it is clearly not related to a glycemic threshold.
Some athletes develop symptoms similar to those of hypoglycemia, even though they aren’t always linked to actual low glycemia. To minimize these symptoms, for these subjects an individual approach is advisable. It may include:
carbohydrate ingestion just before the onset of exercise or during warm-up;
choose low-to-moderate GI carbohydrates that result in more stable glycemic and insulinemic responses;
An high-carbohydrate diet in the days before exercise, as well as ingestion of meals high in carbohydrate 3-4 h before exercise, better if with low glycemic index, can have positive effects on athlete’s performance.
For many years it has been suggested that ingestion of carbohydrates 30-60 min before exercise may adversely affect performance because it could cause hypoglycemia (blood glucose < 3.5 mmol/l or < 63 mg/l), a major contributor to fatigue. In fact, a typical athlete’s mantra is: “Avoid carbohydrate in the hour before exercise”! What is the reason of that? Glucose ingestion may cause hyperglycaemia followed by hyperinsulinaemina that may result in:
a rapid decline in glycemia 15-30 minutes after the onset of exercise, called rebound or reactive hypoglycaemia, most likely the result of:
I. an increase in muscle glucose uptake (due to the mobilization of GLUT-4 transporters by the action of insulin but also from physical activity itself);
II. the reduction in liver glucose output;
in addition, higher availability of carbohydrates to the muscle stimulates glycolysis and this, in combination to insulin-induced inhibition of lipolysis in both adipose tissue and muscle, results in a reduction in fat oxidation (apparently long-chain fatty acids, not medium-chain fatty acids). This may lead to premature glycogen depletion and early onset of fatigue (glycogen would be almost the only available fuel for working muscle).
This effect is temporary, approximately lasting only for the first 20 min of exercise so, it is likely that this little glycogen breakdown has no significant effect on exercise performance.
Therefore, at least in theory, carbohydrate ingestion 60 minutes before exercise could affect performance but only two studies (Foster et al. 1979, e Kovisto et al. 1981) have reported a reduced endurance capacity while the majority of studies have reported no change or an improvement in performance.
To clarify these results, a systematic series of studies was done in trained subjects. The conclusion of these studies was that:
“There is no effect of pre-exercise carbohydrate feeding on performance, even though in some cases hypoglycaemia did develop”.
Ingestion of meals rich in carbohydrates 3-4 h before exercise is important for the increase of liver and muscle glycogen stores, or for their resynthesis in previously depleted muscle and liver. Carbohydrate ingestion 30-60 min before exercise may be important in topping-up liver glycogen stores which serve to maintain blood glucose concentrations during exercise.
Based on the currently available scientific evidences, there is no reason to avoid carbohydrates 60 min before the onset of exercise, because they don’t seem to have any detrimental effect on performance.
During endurance exercise, the most likely contributors to fatigue are dehydration andcarbohydrate depletion, especially of muscle and liver glycogen.
To prevent the “crisis” due to the depletion of muscle and liver carbohydrates, it is essential having high glycogen stores before the start of the activity.
What does affect glycogen stores?
The diet in the days before the competition.
The level of training (well-trained athletes synthesize more glycogen and have potentially higher stores, because they have more efficient enzymes).
The activity in the day of the competition and the days before (if muscle doesn’t work it doesn’t lose glycogen). Therefore, it is better to do light trainings in the days before the competition, not to deplete glycogen stores, and to take care of nutrition.
The “Swedish origin” of carbohydrate loading
Very high muscle glycogen levels (the so-called glycogen supercompensation) can improve performance, i.e. time to complete a predetermined distance, by 2-3% in the events lasting more than 90 minutes, compared with low to normal glycogen, while benefits seem to be little or absent when the duration of the event is less than 90 min.
Well-trained athletes can achieve glycogen supercompensation without the depletion phase prior to carbohydrate loading, the old technique discovered by two Swedish researchers, Saltin and Hermansen, in 1960s.
The researchers discovered that muscle glycogen concentration could be doubled in the six days before the competition following this diet:
three days of low carb menu (a nutritional plan very poor in carbohydrates, i.e. without pasta, rice, bread, potatoes, legumes, fruits etc.);
This diet causes a lot of problems: the first three days are very hard and there may be symptoms similar to depression due to low glucose delivery to brain, and the benefits are few.
Moreover, with the current training techniques, the type and amount of work done, we can indeed obtain high levels of glycogen: above 2.5 g/kg of body weight.
The “corrent” carbohydrate loading
If we compete on Sunday, a possible training/nutritional plan to obtain supercompensation of glycogen stores can be the following:
Wednesday, namely four days before the competition, moderate training and then dinner without carbohydrates;
from Thursday on, namely the three days before the competition, hyperglucidic diet and light trainings.
The amount of dietary carbohydrates needed to recover glycogen stores or to promote glycogen loading depends on the duration and intensity of the training programme, and they span from 5 to 12 g/kg of body weight/d, depending on the athlete and his activity. With higher carbohydrate intake you can achieve higher glycogen stores but this does not always results in better performance; moreover, it should be noted that glycogen storage is associated with weight gain due to water retention (approximately 3 g per gram of glycogen), and this may not be desirable in some sports.
Life depends on appropriate pH levels around and in living organisms and cells.
We requires a tightly controlled pH level in our serum of about 7.4 (a slightly alkaline range of 7.35 to 7.45) to avoid metabolic acidosis and survive. As a comparison, in the past 100 years the pH of the ocean has dropped from 8.2 to 8.1 because of increasing carbon dioxide (CO2) deposition with a negative impact on life in the ocean (it may lead to the collapse of the coral reefs).
Even the mineral content of the food we eat (minerals are used as buffers to maintain pH within the aforementioned range) is considerabled influence by the pH of the soil in which plants are grown. The ideal pH of soil for the best overall availability of essential nutrients is between 6 and 7: an acidic soil below pH of 6 may have reduced magnesium and calcium, and soil above pH 7 may result in chemically unavailable zinc, iron, copper and manganese.
Metabolic acidosis and agricultural and industrial revolutions
In the human diet, there has been considerable change from the hunter gather civilization to the present in the pH and net acid load. With the agricultural revolution (last 10,000 years) and even more recently with industrialization (last 200 years) it has been seen:
an increase in sodium compared to potassium (the ratio potassium/sodium has reversed from 10 to 1 to a ratio of 1 to 3 in the modern diet) and in chloride compared to bicarbonate in the diet,;
This results in a diet that may induce metabolic acidosis which is mismatched to the genetically determined nutritional requirements.
Moreover, with aging, there is a gradual loss of renal acid-base regulatory function and a resultant increase in diet-induced metabolic acidosis.
Finally, a high protein low-carbohydrate diet with its increased acid load results in very little change in blood chemistry, and pH, but results in many changes in urinary chemistry: urinary calcium, undissociated uric acid, and phosphate are increased, while urinary magnesium, urinary citrate and pH are decreased.
All this increases the risk for kidney stones.
pH as a protective barrier
The human body has an amazing ability to maintain a steady pH in the blood with the main compensatory mechanisms being renal and respiratory.
The pH in the body vary considerably from one area to another. The highest acidity is found in the stomach (pH of 1.35 to 3.5) and it aids in digestion and protects against opportunistic microbial organisms. The skin is quite acidic (pH 4-6.5) and this provides an acid mantle as a protective barrier to the environment against microbial overgrowth (this is also seen in the vagina where a pH of less than 4.7 protects against microbial overgrowth).
The urine have a variable pH from acid to alkaline depending on the need for balancing the internal environment.
Fenton T.R., Lyon A.W., Eliasziw M., Tough S.C., Hanley D.A. Meta-analysis of the effect of the acid-ash hypothesis of osteoporosis on calcium balance. J Bone Miner Res 2009;24(11):1835-40 [Abstract]
Fenton T.R., Lyon A.W., Eliasziw M., Tough S.C., Hanley D.A. Phosphate decreases urine calcium and increases calcium balance: a meta-analysis of the osteoporosis acid-ash diet hypothesis. Nutr J 2009;8:article 41 [Abstract]
Fenton T.R., Tough S.C., Lyon A.W., Eliasziw M., Hanley D.A. “Causal assessment of dietary acid load and bone disease: a systematic review and meta-analysis applying Hill’s epidemiologic criteria for causality.” Nutr J 2011;10:article 41 [Abstract]
Schwalfenberg G.K. The alkaline diet: is there evidence that an alkaline pH diet benefits health? J Environ Public Health 2012; Article ID 727630:7 pages doi:10.1155/2012/727630 [Abstract]
In the last years endurance sports, defined in the PASSCLAIM document of the European Commission as those lasting 30 min or more, are increasing in popularity and competitions as half marathons, marathons, even ultramarathons, half Ironmans, or Ironman competitions attract more and more people.
They are competitions which can last hours, or days in the more extreme case of ultramarathons.
Athletes at all levels should take care of training and nutrition to optimize performance and to avoid potential health threats.
In endurance sports the most likely contributors to fatigue are dehydration and carbohydrate depletion (especially liver and muscle glycogen).
Dehydration and endurance sports
Dehydration is due to sweat losses needed to dissipate the heat that is generated during exercise. To prevent the onset of fatigue from this cause, the nutritional target is to reduce sweat losses to less than 2–3% of body weight; it is equally important to avoid drinking in excess of sweating rate, especially low sodium drinks, to prevent hyponatraemia (low serum sodium levels).
Glycogen depletion and endurance sports
Muscle glycogen and blood glucose are the most important substrates from which muscle obtains the energy needed for contraction.
Fatigue during prolonged exercise is often associated with reduced blood glucose levels and muscle glycogen depletion; therefore, it is essential starting exercise/competition with high pre-exercise muscle and liver glycogen concentrations, the last one for the maintaining of normal blood glucose levels.
Other problems which reduce performance and can be an health threat of the athlete, especially in long-distance races, are gastrointestinal problems, hyperthermia and hyponatraemia.
Hyponatraemia has occasionally been reported, especially among slower competitors with very high intakes of low sodium drinks.
Gastrointestinal problems occur frequently, especially in long-distance races; both genetic predisposition and the intake of highly concentrated carbohydrate solutions, hyperosmotic drinks, as well as the intake of fibre, fat, and protein seem to be important in their occurrence.
Carbohydrate mouth rinse and performance responses
The importance of carbohydrates as an energy source for exercise is well known: one of the first study to hypothesize and recognize their importance was the study of Krogh and Lindhardt at the beginning of the 20th century (1920); later, in the mid ‘60’s, Bergstrom and Hultman discovered the crucial role of muscle glycogen on endurance capacity.
Nowdays, the ergogenic effects of carbohydrate supplementation on endurance performance are well known; they are mediated by mechanisms such as:
the maintenance of glycemia and rates of carbohydrate oxidation;
the stimulation of glycogen synthesis during low-intensity exercise ;
a possible stimulatory effect on the central nervous system.
However, their supplementation, immediately before and during exercise, has an improving effect also during exercise (running or cycling) of a shorter and more intense nature: >75% VO2max (maximal oxygen consumption) and ≤1 hour, during which euglycaemia is rarely challenged and adequate muscle glycogen store remains at the cessation of the exercise.
Hypothesis for carbohydrate mouth rinse
In the absence of a clear metabolic explanation it was speculated that ingesting carbohydrate solutions may have a ‘non-metabolic’ or ‘central effect’ on endurance performance. To explore this hypothesis many studies have investigated the performance responses of subjects when carbohydrate solutions (about 6% carbohydrate, often maltodextrins) are mouth rinsed during exercise, expectorating the solution before ingestion.
By functional magnetic resonance imaging and transcranial stimulation it was shown that carbohydrates in the mouth stimulate reward centers in the brain and increases corticomotor excitability, through oropharyngeal receptors which signal their presence to the brain.
Probably salivary amylase releases very few glucose units from maltodextrins which is probably what is needed in order to activate the purported carbohydrate receptors in the oropharynx (no glucose transporters in the oropharynx are known).
However, the performance response appears to be dependent upon the pre-exercise nutritional status of the subject: most part of the studies showing an improving effect on performance was conducted in a fasted states (3- to 15-h fasting).
Only one study has shown improvements of endurance capacity in both fed and fasted states by carbohydrate mouth rinse, but in non-athletic subjects.
Beelen M., Berghuis J., Bonaparte B., Ballak S.B., Jeukendrup A.E., van Loon J. Carbohydrate mouth rinsing in the fed state: lack of enhancement of time-trial performance. Int J Sport Nutr Exerc Metab 2009;19(4):400-9 [Abstract]
Bergstrom J., Hultman E. A study of glycogen metabolism during exercise in man. Scand J Clin Invest 1967;19:218-28 [Abstract]
Bergstrom J., Hultman E. Muscle glycogen synthesis after exercise: an enhancing factor localized in muscle cells in man. Nature 1966;210:309-10 [Abstract]
Painelli V.S., Nicastro H., Lancha A. H.. Carbohydrate mouth rinse: does it improve endurance exercise performance? Nutrition Journal 2010;9:33 [Abstract]
Fares E.J., Kayser B. Carbohydrate mouth rinse effects on exercise capacity in pre- and postprandial States. J Nutr Metab 2011;385962. doi: 10.1155/2011/385962. Epub 2011 Jul 27 [Abstract]
Krogh A., Lindhard J. The relative value of fat and carbohydrate as sources of muscular energy. Biochem J 1920;14:290-363 [PDF]
Rollo I. Williams C. Effect of mouth-rinsing carbohydrate solutions on endurance performance. Sports Med. 2011;41(6):449-61 [Abstract]
Glycogen is an homopolysaccharide formed by units of glucose. Chemically similar to amylopectin, and therefore sometimes referred to as animal starch, compared to the latter it is more compact, extensively branched and larger, reaching a molecular weight up to 108 Da corresponding to about 600000 glucose molecules.
As in the amylopectin, glucose units in the main chain and in the lateral chains are linked by α-(1→4) glycosidic bonds. Lateral chains are joined to the main chain by an α-(1→6) glycosidic bond; unlike amylopectin branches are more frequent, approximately every 10 glucose units (rather than every 25-30 as in amylopectin) and are formed by a smaller numbers of glucose units.
Glycogen is located in the cytosol of the cell in the form of hydrated granules of diameter between 1 to 4 µm and forms complexes with regulatory proteins and enzymes responsible for its synthesis and degradation.
Functions of glycogen
Glycogen, discovered in 1857 by French physiologist Claude Bernard, is the storage form of glucose, and therefore of energy, in animals in which it is present in the liver, muscle (skeletal and heart muscle) and in lower amounts in nearly all the other tissues and organs.
In humans it represents less than 1% of the body’s caloric stores (the other form of caloric reserve, much more abundant, is triacylglycerols stored in adipose tissue) and is essential for maintaining normal glycemia too.
It represents about 10% of liver weight and 1% of muscle weight; although it is present in a higher concentration in the liver, the total stores in muscle are much higher thanks to its greater mass (in a non-fasting 70 kg adult male there are about 100 g of glycogen in the liver and 250 g in the muscle).
Liver glycogen stores is a glucose reserve that hepatocyte releases when needed to maintain a normal blood sugar levels: if you consider glucose availability (in a non-fasting 70 kg adult male) there is about 10 grams or 40 kcal in body fluids while hepatic glycogen can supply, also after a fasting night, about 600 kcal.
In skeletal and cardiac muscle, glucose from glycogen stores remains within the cell and is used as an energy source for muscle work.
The brain contains a small amount of glycogen, primarily in astrocytes. It accumulates during sleep and is mobilized upon waking, therefore suggesting its functional role in the conscious brain. These glycogen reserves also provide a moderate degree of protection against hypoglycemia.
It has a specialized role in fetal lung type II pulmonary cells. At about 26 weeks of gestation these cells start to accumulate glycogen and then to synthesize pulmonary surfactant, using it as a major substrate for the synthesis of surfactant lipids, of which dipalmitoylphosphatidylcholine is the major component.
Glycogen and foods
It is absent from almost all foods because after an animal is killed it is rapidly broken down to glucose and then to lactic acid; it should be noted that the acidity consequently to lactic acid production gradually improves the texture and keeping qualities of the meat. The only dietary sources are oysters and other shellfish that are eaten virtually alive: they contain about 5% glycogen.
In humans, accumulation of glycogen is associated with weight gain due to water retention: for each gram of stored glycogen 3 grams of water are retained.
Arienti G. “Le basi molecolari della nutrizione”. Seconda edizione. Piccin, 2003
Cozzani I. and Dainese E. “Biochimica degli alimenti e della nutrizione”. Piccin Editore, 2006
Giampietro M. “L’alimentazione per l’esercizio fisico e lo sport”. Il Pensiero Scientifico Editore, 2005
So, the best strategy for losing body fat is not a drastic reduction in caloric intake, nor follow constrictive or “strange” diets, such as hcg diet plan, sacred heart diet, paleo diet, Master Cleanse diet (the diet that Beyonce did), etc., that require to eliminate or greatly reduce the intake of certain macronutrients, mostly carbohydrates.
Such conducts can be:
very stressful from psychological point of view;
not passable for long periods;
hazardous to health because of inevitable nutrient deficiencies.
Finally, they do not ensure that all the weight lost is only or almost only body fat and are often followed by substantial increases in body weight (weight cycling or yo-yo effect).
An excessive reduction of energy intake means eating very little and this determines the risk, high, not to take adequate amounts of the various essential nutrients, that is, what we can’t synthesize, such as vitamins, certain amino acids, some fatty acids and minerals, including e.g. calcium, essential for bone metabolism at every stage of life, or iron, used in many body functions as the transport of oxygen to the tissues. This results in a depression of metabolism and hence a reduction in energy expenditure.
Whether the reduction in energy intake is excessive, or even there are periods of fasting, it adds insult to injury because a proportion of free fatty mass will be lost. How?
Body fat, reduction in energy intake and role of carbohydrates
Glucose is the only energy source for red blood cells and some brain areas, while other brain areas can also derive energy from ketone bodies, which are a product of fatty acid metabolism.
At rest, brain extracts 10% of the glucose from the bloodstream, a significant amount, about 75 mg/min., considering that its weight is about 1.5 kg. To maintain a constant glycemia, and thus ensure a constant supply of glucose to tissues, we needs to take carbohydrates or alternatively amino acids, both easily obtained from foods.
In the case of a low or absent dietary intake of carbohydrates, whereas after about 18 hours liver glycogen, which releases glucose into circulation, depletes, body synthesizes de novo glucose from certain amino acids through a process called gluconeogenesis (actually this metabolic pathway is active even after a normal meal but increases its importance in fasting).
But what’s the main source of amino acids in the body when their dietary intake is low or absent? Endogenous proteins, and there is a hierarchy in their use that is before we consume the less important and only after the most important ones. For the first digestive enzymes, pepsin, chymotrypsin, elastase, carboxypeptidase and aminopeptidase (around 35-40 g) will be used; successively liver and pancreas slow down their synthesis activities for export proteins and unused amino acids are directed to gluconeogenesis. It’s clear that these are quite modest reserves of amino acids and it is the muscle that will undertake to provide the required amounts of amino acids that is proteolysis of muscleproteins begins.
Note: Anyway, there is no absolute sequentiality in the degradation of several proteins, there is instead a plot in which, proceeding, some ways lose their importance and others will buy. So, to maintain constant glycemia the protein component of muscle is reduced, including skeletal muscle that is a tissue that represents a fairly good portion of the value of the basal metabolism and that, with exercise, can significantly increase its energy consumption: thus essential for weight loss and subsequent maintenance. It is as if the engine capacity was reduced.
One thing which we don’t think about is that heart is a muscle that may be subject to the same processes seen for skeletal muscle.
Ultimately make glucose from proteins, also food-borne, is like heat up the fire-place burning the furniture of the eighteenth century, amino acids, having available firewood, dietary carbohydrates.
Therefore, an adequate intake of carbohydrates with diet prevents excessive loss of proteins, namely, there is a saving effect of proteins played by carbohydrates.
Mammals, and therefore humans, can’t synthesize glucose from fats.
The elimination or substantial reduction in carbohydrate intake in the diet results in an increased intake of proteins, fats and cholesterol because it will increase the intake of animal products, one of the main defects in hyperproteic diet.
In the body there are no amino acids reserves, thus they are metabolized and, as a byproduct of their use, ammonia is formed and it’ll be eliminated as toxic. For this reason high-protein diets imply an extra work for liver and kidneys and also for this they are not without potential health risks.
An increased fat intake often results into an increased intake of saturated and trans fats and cholesterol, with all the consequences this may have on cardiovascular health.
What has been said so far should not induce to take large amounts of carbohydrates; this class of macronutrients should represent 55-60% of daily calories, fats 25-30% (primarily extra-virgin olive oil) and the remainder proteins: thus a composition in macronutrient that refers to prudent diet or Mediterranean Diet.
Body fat and the entry in a phase of famine/disease
A excessive reduction in caloric intake is registered by our defense mechanisms as an “entry” in a phase of famine/disease.
The abundance of food is a feature of our time, at least in industrialized countries, while our body evolved over hundreds of thousands of years during which there was no current abundance: so it’s been programmed to try to overcome with minimal damage periods of famine. If caloric intake is drastically reduced it mimics a famine: what body does is to lower consumption, lower the basal metabolism, that is, consumes less and therefore also not eating much we will not get great results. It is as if a machine is lowered the displacement, it’ll consume less (our body burns less body fat).
In summary, the best way to lose body fat, that also protects against future increases, is to make negative the daily caloric balance increasing physical activity and controlling food intake, i.e. change your own lifestyle.
Cereda E., Malavazos A.E., Caccialanza R., Rondanelli M., Fatati G. and Barichella M. Weight cycling is associated with body weight excess and abdominal fat accumulation: a cross-sectional study. Clin Nutr 2011;30(6):718-23. doi:https://doi.org/10.1016/j.clnu.2011.06.009
Giampietro M. L’alimentazione per l’esercizio fisico e lo sport. Il Pensiero Scientifico Editore. Prima edizione 2005
Ravussin E., Lillioja S., Knowler W.C., Christin L., Freymond D., Abbott W.G.H., Boyce V., Howard B.V., and Bogardus C. Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med 1988;318:467-72.doi:10.1056/NEJM198802253180802
Sachiko T. St. Jeor S.T. St., Howard B.V., Prewitt T.E., Bovee V., Bazzarre T., Eckel T.H., for the AHA Nutrition Committee. Dietary Protein and Weight Reduction. A Statement for Healthcare Professionals From the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation 2001;104:1869-74. doi:https://doi.org/10.1161/hc4001.096152
An important energy source for working muscle is its glycogen store, whose level is correlated with the onset of fatigue.
The highly trained athlete not only has glycogen stores potentially higher but he is also able to synthesize it faster thanks to more efficient enzymes.
To synthesize glycogen it is necessary to ingest carbohydrates; but how many, which, when, and how often?
The two phases of muscle glycogen synthesis after exercise
In order to restore as quickly as possible muscle glycogen depots, it is useful to know that, as a result of training sessions that deplete muscle glycogento values below 75% those at rest and not fasting, glycogen synthesis occurs in two phases.
To know and therefore take advantage of the biphasicity is important for those athletes who are engaged in more daily training sessions, or who otherwise have little time for recovery between a high intensity exercise and the subsequent one (less than 8 hours), in order to maximize glycogen synthesis and achieve the optimal performance during a second close exercise session.
The two phases are characterized by:
a different sensitivity to circulating insulin levels;
Muscle glycogen synthesis after exercise: the first phase
The first phase, immediately following the end of an activity and lasting 30-60 minutes, is insulin-independent, i.e. glucose uptake by muscle cell as glycogen synthesis are independent from hormone action.
This phase is characterized by an elevated rate of synthesis that however decreases rapidly if you do not take in carbohydrates: the maximum rate is in the first 30 minutes, then declines to about one fifth in 60 minutes, and to about one ninth in 120 minutes from the end of exercise.
How is it possible to take advantage of this first phase to replenish muscle glycogen stores as much as possible? By making sure that the greatest possible amount of glucose arrives to muscle in the phase immediately following to the end of exercise, best if done within the first 30 minutes.
What to ingest?
High glycemic index, but easy to digest and absorb, carbohydrates.
Therefore, it is advisable to replace foods, even though of high glycemic index, that need some time for digestion and the subsequent absorption, with solutions/gel containing for example glucose and/or sucrose. These solutions ensure the maximal possible absorption rate and resupply of glucose to muscle because of they contain only glucose and are without fiber or anything else that could slow their digestion and the following absorption of the monosaccharide, that is, they are capable of producing high blood glucose levels in a relatively short time.
It is also possible to play on temperature and concentration of the solution to accelerate the gastric transit.
It should be further underlined that the use of these carbohydrate solutions is recommended only when the recovery time from a training/competition session causing significant depletion of muscle glycogen and the following one is short, less than 8 hours.
How many carbohydrates do you need?
Many studies has been conducted to find the ideal amount of carbohydrates to ingest.
If in post-exercise the athlete does not eat, glycogen synthesis rate is very low, while if he ingests adequate amounts of carbohydrates immediately after cessation of exercise, synthesis rate can reach a value over 20 times higher.
From the analysis of scientific literature it seems reasonable to state that, as a result of training sessions that deplete muscle glycogen stores as seen above (<75% of those at rest and not fasting), the maximum synthesis rate is obtained by carbohydrate intake, with high glycemic index and high digestion and absorption rates, equal to about 1.2 g/kg of body weight/h for the next 4-5 hours from the end of exercise.
In this way, the amount of glycogen produced is higher than 150% compared to the ingestion of 0.8 g/kg/h.
Because further increases, up to 1.6 g/kg/h, do not lead to further rise in glycogen synthesis rate, the carbohydrate amount equal to 1.2 g/kg/h can be considered optimum to maximize the resynthesis rate of muscle glycogen stores during post-exercise.
And the frequency of carbohydrate ingestion?
It was observed that if carbohydrates are ingested frequently, every 15-30 minutes, it seems there is a further stimulation of muscle glucose uptake as of muscle glycogen replenishment compared with ingestion at 2-hours intervals. Particularly, ingestions in the first post-exercise hours seem to optimize glycogen levels.
Muscle glycogen synthesis after exercise: the second phase
The second phase begins from the end of the first, lasts until the start of the last meal before the next exercise (hence, from several hours to days), and is insulin-dependent i.e. muscle glucose uptake and glycogen synthesis are sensitive to circulating hormone levels.
Moreover, you observe a significant reduction in muscle glycogen synthesis rate: with adequate carbohydrate intake the synthesis rate is at a value of about 10-30% lower than that observed during the first phase.
This phase can last for several hours, but tends to be shorter if:
In order to optimize the resynthesis rate of glycogen, experimental data indicate that meals with high glycemic index carbohydrates are more effective than those with low glycemic index carbohydrates; but if between a training/competition session and the subsequent one days and not hours spend, the evidences do not favor high glycemic index carbohydrates as compared to low glycemic index ones as long as an adequate amount is taken in.
Muscle glycogen synthesis rate and ingestion of carbohydrates and proteins
The combined ingestion of carbohydrates and proteins (or free insulinotropic amino acids) allows to obtain post-exercise glycogen synthesis rate that does not significantly differ from that obtained with larger amounts of carbohydrates alone. This could be an advantage for the athlete who may ingest smaller amount of carbohydrates, therefore reducing possible gastrointestinal complications commons during training/competition afterward to their great consumption.
From the analysis of scientific literature it seems reasonable to affirm that, after an exercise that depletes at least 75% of muscle glycogen stores, you can obtain a glycogen synthesis rate similar to that reached with 1.2 g/kg/h of carbohydrates alone (the maximum obtainable) with the coingestion of 0.8 g/kg/h of carbohydrates and 0.4 g/kg /h of proteins, maintaining the same frequency of ingestion, therefore every 15-30 minutes during the first 4-5 hours of post-exercise.
However, the molecular mechanisms underlying these changes are different.
In the first phase, the increase in glucose transport rate, independent from insulin presence, is mediated by the translocation, induced by the contraction, of glucose transporters, called GLUT4, on the cytoplasmatic membrane of the muscle cell.
In addition, the low glycogen levels also stimulate glucose transport as it is believed that a large portion of transporter-containing vesicles are bound to glycogen, and therefore they may become available when its levels are depleted.
Finally, the low muscle glycogen levels stimulate glycogen synthase activity too: it has been demonstrated that these levels are a regulator of enzyme activity far more potent than insulin.
In the second phase, the increase in muscle glycogen synthesis is due to insulin action on glucose transporters and on glycogen synthase activity of muscle cell. This sensibility to the action of circulating insulin, that can persist up to 48 hours, depending on carbohydrate intake and the amount of resynthesized muscle glycogen, has attracted much attention: it is in fact possible, through appropriate nutritional intervention, to increase the secretion in order to improve glycogen synthesis itself, but also protein anabolism, reducing at the same time the protein-breakdown rate.
The coingestion of carbohydrates and proteins (or free amino acids) increases postprandial insulin secretion compared to carbohydrates alone (in some studies there was an increase in hormone secretion 2-3 times higher compared to carbohydrates alone).
It was speculated that, thanks to the higher circulating insulin concentrations, further increases in post-exercise glycogen synthesis rate could be obtained compared to those observed with carbohydrates alone, but in reality it does not seem so. In fact, if carbohydrate intake is increased to 1.2 g/kg/h plus 0.4 g/kg/h of proteins no further increases in glycogen synthesis rate are observed if compared to those obtained with the ingestion of carbohydrates alone in the same amount (1,2 g/kg/h, that, as mentioned above, like the coingestion of 0,8 g/kg/h of carbohydrates and 0,4 g/kg/h of proteins, allows to attain the maximum achievable rate in post-exercise) or in isoenergetic quantities, that is, 1.6 g/kg (proteins and carbohydrates contain the same calorie/g)
The greater circulating insulin levels reached with the coingestion of carbohydrates and proteins (or free amino acids) might stimulate the accumulation of ingested carbohydrates in tissues most sensitive to its action, such as liver and previously worked muscle, thus resulting in a more efficient storage, for the purposes of sport activity, of the same carbohydrates.
Beelen M., Burke L.M., Gibala M.J., van Loon J.C. Nutritional strategies to promote postexercise recovery. Int J Sport Nutr Exerc Metab 2010:20(6);515-32 doi:10.1123/ijsnem.20.6.515
Berardi J.M., Noreen E.E., Lemon P.W.R. Recovery from a cycling time trial is enhanced with carbohydrate-protein supplementation vs. isoenergetic carbohydrate supplementation. J Intern Soc Sports Nutrition 2008;5:24 doi:10.1186/1550-2783-5-24
Betts J., Williams C., Duffy K., Gunner F. The influence of carbohydrate and protein ingestion during recovery from prolonged exercise on subsequent endurance performance. J Sports Sciences 2007;25(13):1449-60 doi:10.1080/02640410701213459
Howarth K.R., Moreau N.A., Phillips S.M., and Gibala M.J. Coingestion of protein with carbohydrate during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans. J Appl Physiol 2009:106;1394–1402 doi:10.1152/japplphysiol.90333.2008
Jentjens R., Jeukendrup A. E. Determinants of post-exercise glycogen synthesis during short-term recovery. Sports Medicine 2003:33(2);117-144 doi:10.2165/00007256-200333020-00004
Millard-Stafford M., Childers W.L., Conger S.A., Kampfer A.J., Rahnert J.A. Recovery nutrition: timing and composition after endurance exercise. Curr Sports Med Rep 2008;7(4):193-201 doi:10.1249/JSR.0b013e31817fc0fd
Price T.B., Rothman D.L., Taylor R., Avison M.J., Shulman G.I., Shulman R.G. Human muscle glycogen resynthesis after exercise: insulin-dependent and –independent phases. J App Physiol 1994:76(1);104–111 doi:10.1152/jappl.19220.127.116.11
van Loon L.J.C., Saris W.H.M., Kruijshoop M., Wagenmakers A.J.M. Maximizing postexercise muscle glycogen synthesis: carbohydrate supplementation and the application of amino acid or protein hydrolysate mixtures. Am J Clin Nutr 2000;72: 106-111 doi:10.1093/ajcn/72.1.106
Biochemistry and Nutrition