Strategies to maximize muscle glycogen resynthesis after exercise

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.

Glycogen
Fig. 1 – Glycogen Structure

To synthesize glycogen it is necessary to ingest carbohydrates; but how many, which, when, and how often?

CONTENTS

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 glycogen to 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;
  • a different velocity.

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.

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.

The two phases: molecular mechanisms

The biphasicity is consequence, in both phases, of an increase in:

  • glucose transport rate into cell;
  • the activity of glycogen synthase, the enzyme that catalyzes glycogen synthesis.

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.

Glycogen synthesis rate and insulin

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)

Insulin and preferential carbohydrate storage

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.

References

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.1994.76.1.104

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

Skeletal muscle glycogen stores and sports

Muscle glycogen represents a source of glucose, therefore energy, that can be used by muscle during physical activity: it is an energy store where needed!
Furthermore a close relationship exists between the onset of fatigue and depletion of its muscle stores.

Glycogen as energy source

Carbohydrates and fatty acids represent the main energy source for muscle during exercise and their relative contribution varies depending on:

  • the intensity and duration of exercise;
  • the level of training.

Skeletal Muscle GlycogenIf for fatty acids there are no problems regarding body stores so it is not for carbohydrates whose stores, present in glycogen form principally in the liver and the muscle, are modest, less than 5% of total body energy stores: in a non-fasting 70 kg adult male there are about 250 g of glycogen in the muscle and 100 g in the liver, for a total energy of about 1400 kcal. In athletes the amount could be higher, for example in the best marathoners, again considering an adult male as above, you can reach up to 475 g in total, muscle plus liver, which corresponds to about 1900 kcal.
In spite of this, glycogen contribution to the total energy needed to sustain muscular workload rises with the increase of exercise intensity, whereas we reduce that in the form of fatty acids.
Furthermore, in the absence of replenishment with exogenous carbohydrates, performance is determined by the endogenous stores of liver and skeletal muscle glycogen, of which relative consumption is different: an increase of intensity increases that of the second (muscle) while remain more or less constant in that of the first (liver).

Skeletal muscle glycogen and intese exercises

In fact, skeletal muscle glycogen represents the most important energy reserve for prolonged moderate-high intensity exercise, an importance that increase in the case of high-intensity interval exercise (common in training session undertaken by swimmers runners, rowers or in team-sport players) or in resistance exercise, therefore both endurance and resistance exercises. If for example we consider the marathon about 80% of utilized energy derives from carbohydrate oxidation, for the most part skeletal muscle glycogen.
Finally, the replenishment rate of glycogen stores in post-exercise is one of the most important factors in establishing necessary recovery time.

Muscle glycogen and fatigue

Fatigue and low glycogen levels are closely correlate but it is not clear which mechanisms are at the basis of this relationship; one hypothesis is that there exists a minimum glycogen concentration that is “protected” and is resistant to being used during exercise, perhaps to ensure an energy reserve in case of extreme necessity.
Because of the closely relationship between skeletal muscle glycogen depletion and fatigue, its replenish rate in the post-exercise is one of the most important factors in determining necessary recovery time.

References

Arienti G. “Le basi molecolari della nutrizione”. Seconda edizione. Piccin, 2003

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

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

Mahan LK, Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Mariani Costantini A., Cannella C., Tomassi G. “Fondamenti di nutrizione umana”. 1th ed. Il Pensiero Scientifico Editore, 1999

Nelson D.L., M. M. Cox M.M. Lehninger. Principles of biochemistry. 4th Edition. W.H. Freeman and Company, 2004

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

Daily protein requirements for athletes

Proteins Requirements
Fig. 1 – Food High in Proteins

It is now accepted by athletes, coaches and athletic trainers that proper diet is one of the cornerstones for achieving better athletic performance. Despite this widely spread assumption, many, even at the highest levels, still believe that an high protein intake is fundamental in the athlete’s diet. This opinion is not new and is deeply rooted in the imaginary of many people almost as if, eating meat, even of big and strong animals, we were able to gain their strength and vitality too.
The function of proteins as energy-supplier for working muscle was hypothesized for the first time by von Liebig in ‘800 and it is because of his studies if, even today, animal proteins, and therefore meats, are often believed having great importance in the energy balance in the athlete’s diet, despite nearly two centuries in which biochemistry and sports medicine have made enormous progress.
Really, by the end of ‘800 von Pettenkofer and Voit and, at the beginning of ‘900, Christensen and Hansen retrenched their importance for energy purposes, also for the muscle engaged in sport performance, instead bringing out the prominent role played by carbohydrates and lipids.
Of course we shouldn’t think that proteins are not useful for the athlete or sedentary people. The question we need to answer is how many proteins a competitive athlete, engaged in intense and daily workouts, often two daily sessions (for 3-6 hours), 7/7, for more than 10 months a year, needs per day. We can immediately say that, compared to the general population, and with the exception of some sports, (see below) the recommended amount of protein is greater.

Metabolic fate of proteins at rest and during exercise

In a healthy adult subject engaged in a non-competitive physical activity, the daily protein requirements is about 0.85 g/kg desirable body weight, as shown by WHO.
Proteins turnover in healthy adults, about 3-4 g/kg body weight/day (or 210-280 g for a 70 kg adult), is slower for the muscle than the other tissues and decreasing with age, and is related to the amount of amino acids in the diet and protein catabolism.
At rest the anabolic process, especially of synthesis, uses about 75% amino acids while the remaining 25% undergoes oxidative process, that will lead to CO2 and urea release (for the removal of ammonia).
During physical activity, as result of the decreased availability of sugars, i.e. muscle glycogen and blood glucose used for energy purposes, as well as the intervention of cortisol, the percentage of amino acids destinated to anabolic processes is reduced while it increases that of amino acids diverted to catabolic processes, that is, it occurs an increase in the destruction of tissue proteins.
At the end of physical activity, for about two hours, anabolic processes remain low whereupon it occurs their sharp increase that brings them to values higher than basal ones, so, training induces an increase in protein synthesis even in the absence of an increase in proteins intake.

What determines the daily protein requirements?

There are many factors to be taken into account in the calculation of the daily protein requirements.

  • The age of the subject (if, for example, he/she is in the age of development).
  • Gender: female athletes may require higher levels as their energy intake is lower.
  • An adequate carbohydrate intake reduces their consumption.
    During physical activity, glucogenic amino acids may be used as energy source directly in the muscle, after their conversion to glucose in the liver through gluconeogenesis.
    An adequate carbohydrate intake before and during prolonged exercise lowers the use of body proteins.
  • The amount of carbohydrates stored in muscles and liver (glycogen) (see above).
  • The energy intake of the diet.
    A reduced energy intake increases protein requirements; conversely, the higher energy intake, the lower the amount of protein required to achieve nitrogen balance; usually there is a nitrogen retention of 1-2 mg per kcal introduced.
    If the athlete is engaged in very hard competition/workouts, or if he requires an increase in muscle masses (e.g. strength sports) nitrogen balance must be positive; a negative balance indicates a loss of muscle mass.
    The nitrogen balance is calculated as difference between the nitrogen taken with proteins (equal to: g. proteins/6.25) and the lost one (equal to: urinary urea in 24 hours, in g., x0.56]; in formula:

Nb (nitrogen balance) = (g. protein/6.25) – [urinary urea in 24 hours, in g., x0.56)]

  • The type of competition/workouts that the athlete is doing, either resistance or endurance, as well as the duration and intensity of the exercise itself.
    Resistance training leads to an increase in protein turnover in muscle, stimulating protein synthesis to a greater extent than protein degradation; both processes are influenced by the recovery between a training and the next one as well as by the degree of training (more training less loss).
    In the resistance and endurance performances the optimal protein requirements in younger people as for those who train less time are estimated at 1.3 to 1.5 g protein/kg body weight, while in adult athletes who train more time is slightly lower, about 1-1.2 g/Kg of body weight.
    Why?
    In subjects engaged in a hard physical activity, proteins are used not only for plastic purposes, which are incremented, but also for energy purposes being able to satisfy in some cases up to 10-15% of the total energy demand.
    Indeed, intense aerobic performances, longer than 60 minutes, obtain about 3-5% of the consumed energy by the oxidation of protein substrates; if we add to this the proteins required for the repair of damaged tissue protein structures, it results a daily protein demand about 1.2 to 1.4 g/kg body weight.
    If the effort is intense and longer than 90 minutes (as it may occur in road cycling, running, swimming, or cross-country skiing), also in relation to the amount of available glycogen in muscle and liver (see above), the amount of proteins used for energy purposes can get to satisfy, in the latter stages of a prolonged endurance exercise, 15% of the energy needs of the athlete.
  • The physical condition.
  • When needed, the desired weight.
    Athletes attempting to lose weight or maintain a low weight may need more proteins.

From the above, protein requirements don’t exceed 1.5 g/kg body weight, also for an adult athlete engaged in intense and protracted workouts, while if you consider the amount of protein used for energy purposes, you do not go over 15% of the daily energy needs.
So, it’s clear that diets which supply higher amounts (sometimes much higher) of proteins aren’t of any use, stimulate the loss of calcium in bones and overload of work liver and kidney. Moreover, excess proteins don’t accumulate but are used to fat synthesis.

How to meet the increased protein requirements of athletes

Protein Requirements
Fig. 2 – Road Cycling

A diet that provides 12 to 15% of its calories from protein will be quite sufficient to satisfy the needs of almost all of the athletes, also those engaged in exhausting workouts.
In fact, with the exception of some sports whose energy expenditure is low, close to that of sedentary subject (for example: shooting, or artistic and rhythmic gymnastics), athletes need a high amount of calories and, for some sports such as road cycling, swimming or cross-country skiing, it may be double/triple than that of a sedentary subject.
The increase in food intake is accompanied by a parallel increase in protein intake, because only a few foods such as honey, maltodextrin, fructose, sugar and vegetable oils are protein-free, or nearly protein-free.

Calculation of protein requirements of athletes

If you consider an energy demand of 3500 kcal/die, with a protein intake equal to 15% of total daily calories, you have:

3500 x 0.15 = 525 Kcal

As 1 gram of protein contains 4 calories, you obtain:

525/4 = 131 g of proteins

Dividing the number found by the highest protein requirements seen above (1.5 g/kg body weight/day), you obtain:

131/1.5 = 87 kg

that is, the energy needs of a 87 kg athlete engaged in intense workouts are satisfied.
Repeating the same calculations for a caloric intake of 5000 , you obtain 187 g of protein; dividing it by 1.5 the result is 125 kg, that is, the energy needs of a 125 kg athlete are satisfied.
These protein intakes can be met by a Mediterranean-type diet, without protein or amino acids supplements.

References

Giampietro M. L’alimentazione per l’esercizio fisico e lo sport. Il Pensiero Scientifico Editore. Prima edizione 2005

Protein and amino acid requirements in human nutrition. Report of a joint FAO/WHO/UNU expert consultation. 2002 (WHO technical report series ; no. 935).

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

Omega-6 polyunsaturated fatty acids

Omega-6 polyunsaturated fatty acids are the major polyunsaturated fatty acids (PUFA) in the Western diet (about 90% of all of them in the diet), being components of most animal and vegetable fats.

CONTENTS:

The synthesis of ω-6 polyunsaturated fatty acids

Fig. 1 – Omega Designation System

Within the omega-6 (ω-6) family, linoleic acid is one of the most important and widespread fatty acids and the precursor of all omega-6 polyunsaturated fatty acids. It is produced de novo from oleic acid (an omega-9 fatty acid) only by plant in a reaction catalyzed by Δ12-desaturase, i.e. the enzyme that forms the omega-6 polyunsaturated fatty acid family from omega-9 one.
Δ12-desaturase catalyzes the insertion of the double bond between carbon atoms 6 and 7, numbered from the methyl end of the molecule.


Linoleic acid, together with alpha-linolenic acid, is a primary product of plant polyunsaturated fatty acids synthesis.

Metabolism of Omega-6 Polyunsaturated Fatty Acids
Fig. 2 – Metabolism of Omega-6 Polyunsaturated Fatty Acids

Animals, lacking Δ12-desaturase, can’t synthesize it, and all the omega-6 polyunsaturated fatty acid family de novo, and they are obliged to obtain it from plant foodstuff and/or from animals that eat them; for this reason omega-6 polyunsaturated fatty acid are considered essential fatty acids, so called EFA (the essentiality of omega-6 polyunsaturated fatty acids, in particular just the essentiality of linoleic acid, was first reported in 1929 by Burr and Burr).

ω-6 PUFA: from linoleic acid to arachidonic acid

Animals are able to elongate and desaturase dietary linoleic acid in a cascade of reactions to form very omega-6 polyunsaturated fatty acids.
Linoleic acid is first desaturated to gamma-linolenic acid, another important ω-6 fatty acid with significant physiologic effects, in the reaction catalyzed by Δ6-desaturase. It is thought that the rate of this reaction is limiting in certain conditions like in the elderly, under certain disease states and in premature infants; for this reason, and because it is found in relatively small amounts in the diet, few oils containing it (black currant, evening primrose, and borage oils) have attracted attention.
In turn gamma-linolenic acid may be elongated to dihomo-gamma-linolenic acid by an elongase (it catalyzes the addition of two carbon atoms from glucose metabolism to lengthen the fatty acid chain) that may be further desaturated in a very limited amount to arachidonic acid, in a reaction catalyzed by another rate limiting enzyme, Δ5-desaturase.
Arachidonic acid can be elongated and desaturated to adrenic acid.

It should be noted that polyunsaturated fatty acids in the omega-6 family, and in any other n-families, can be interconverted by enzymatic processes only within the same family, not among families.

C-20 polyunsaturated fatty acids belonging to omega-6 and omega-3 families are the precursors of eicosanoids (prostaglandins, prostacyclin, thromboxanes, and leukotrienes), powerful, short-acting, local hormones.

While the deprivation of omega-3 polyunsaturated fatty acids causes dysfunction in a wide range of behavioral and physiological modalities, the omission in the diet of omega-6 polyunsaturated fatty acids results in manifest systemic dysfunction.

In plant seed oils omega-6 fatty acids with chain length longer than 18 carbons are present only in trace while arachidonic acid is found in all animal tissues and animal-based food products.

References

Akoh C.C. and Min D.B. “Food lipids: chemistry, nutrition, and biotechnology” 3th ed. 2008

Aron H. Uber den Nahvert (On the nutritional value). Biochem Z. 1918;92:211–233 (German)

Bender D.A. “Benders’ dictionary of nutrition and food technology”. 2006, 8th Edition. Woodhead Publishing. Oxford

Bergstroem S., Danielsson H., Klenberg D. and Samuelsson B. The enzymatic conversion of essential fatty acids into prostaglandins. J Biol Chem 1964;239:PC4006-PC4008.

Burr G. and Burr M. A new deficiency disease produced by the rigid exclusion of fat from the diet. J Biol Chem 1929;82:345-67.

Chow Ching K. “Fatty acids in foods and their health implication” 3th ed. 2008

Cozzani I. e Dainese E. “Biochimica degli alimenti e della nutrizione”. Piccin Editore, 2006

Mahan L.K., Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Rosenthal M.D., Glew R.H. Mediacal biochemistry. Human metabolism in health and disease. John Wiley & Sons, Inc. 2009

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

Van D., Beerthuis R.K., Nugteren D.H. and Vonkeman H. Enzymatic conversion of all-cis-polyunsaturated fatty acids into prostaglandins. Nature 1964;203:839-41

Relationship between omega-3, omega-6 and omega-9 PUFA

  • Impair uptake of omega-6 polyunsaturated fatty acids (PUFA).
  • Inhibit desaturases, especially Δ6 desaturase.
  • Competitively inhibit cyclooxygenase and lipoxygenase.
  • Compete with omega-6 polyunsaturated fatty acids for acyltransferases.
  • Dilute pools of free arachidonic acid.
  • Displace arachidonic acid from specific phospholipid pools.
  • Form eicosanoid analogs with less activity or competitively bind to eicosanoid sites.
  • Alter membrane properties and associated enzyme and receptor functions.

Source: adapted from Kinsella, J.E. in Omega-3 Fatty Acids in Health and Disease, R.S. Lees and M. Karel, eds, Dekker, New York, 1990.

Relationship between ω-3 , ω-6 and ω-9 fatty acid families

Relationship between ω-3, ω-6 and ω-9 PUFA
Mackerel

The Δ5 and Δ6 desaturases prefer fatty acids with double bonds in the omega-6 or n-6 and, secondarily, the omega-3 or n-3 position of the carbon chain.
Omega-3 polyunsaturated fatty acid family competitively suppresses, at enzymatic level, the synthesis of the omega-6 polyunsaturated fatty acids; for these reasons relative and absolute dietary intake is important in the determination of tissue omega-3 and omega-6 polyunsaturated fatty acid levels.
Both omega-3 and omega-6 families suppress the formation of the omega-9 polyunsaturated fatty acids.

References

Akoh C.C. and Min D.B. “Food lipids: chemistry, nutrition, and biotechnology” 3th ed. 2008

Bender D.A. “Benders’ dictionary of nutrition and food technology”. 2006, 8th Edition. Woodhead Publishing. Oxford

Chow Ching K. “Fatty acids in foods and their health implication” 3th ed. 2008

Mahan L.K., Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

Omega-3 polyunsaturated fatty acids

Within omega-3 (ω-3) polyunsaturated fatty acid family:

are important fatty acids.

The synthesis of ω-3 polyunsaturated fatty acids

Like linoleic acid (omega-6 fatty acid), alpha-linolenic acid or ALA is a primary product of plant polyunsaturated fatty acid or PUFA synthesis and is the precursor of all the omega-3 polyunsaturated fatty acids.
It is produced de novo from linoleic acid only by plants (by the chloroplasts of marine phytoplankton and land plants) in a reaction catalyzed by Δ15-desaturase, i.e. the enzyme that forms the omega-3 polyunsaturated fatty acid family from omega-6 one catalyzing the insertion of the double bond between carbon atoms 3 and 4, numbered from methyl end of the molecule.


Note: while many land plants lack the ability to synthesize omega-3 polyunsaturated fatty acids, aquatic ones and planktons in colder water produce abundant amounts of them.

Omega-3 Polyunsaturated Fatty Acids: Omega-3 Fatty Acid Metabolism
ω-3 Fatty Acid Metabolism

Animals, lacking Δ15-desaturase, can’t synthesize alpha-linolenic acid, and all the omega-3 polyunsaturated fatty acid family de novo, and they are obliged to obtain it from plant foodstuff and/or from animals that eat them; for this reason omega-3 polyunsaturated fatty acids are considered essential fatty acids, so called EFA.

Omega-3 PUFA: from α-linolenic acid to EPA and DHA

Animals are able to elongate and desaturase dietary alpha-linolenic acid in a cascade of reactions to form very long polyunsaturated omega-3 fatty acids but terrestrial animals have limited ability to do it. The efficiency of synthesis decreases down the cascade: conversion of alpha-linolenic acid to EPA is limited (the activity of Δ6-desaturase is the rate limiting in humans) and to DHA is even more restricted than that of EPA. This metabolic pathway occurs mainly in the liver and cerebral microvasculature of the blood brain barrier, but also in the cerebral endothelium and astrocytes.

Fish and shellfish, unlike terrestrial animals, are able to convert efficiently alpha-linolenic acid, obtained from chloroplast of marine phytoplankton, in EPA and DHA (the last one is present in high concentration in many fish oils but pay attention: many fish oils are also rich in saturated fatty acids).
It should be noted that polyunsaturated fatty acids of the ω-3 family, and of any other n-families, can be interconverted by enzymatic processed only within the same family, not among families.

EPA and DHA are primarily found in marine algae (in genetically engineered algae DHA represents approximately 50% of the total fatty acids), fish, shellfish, and marine products (particularly oil from cold-water marine fish).

Some functions of ω-3 polyunsaturated fatty acids

  • Omega-3 polyunsaturated fatty acid are capable of increasing high-density lipoprotein (HDL), “good cholesterol”, and of interleukin-2 levels. On the other hand, they decrease the levels of low-density lipoprotein (LDL), “bad cholesterol“, and very low density lipoprotein cholesterol (VLDL) and of interleukin-1 levels.
  • They are essential for the normal functioning of the brain and retina, especially in premature borns.
  • They are essential for growth and development throughout the life; for example if in children diet there is not enough omega-3 polyunsaturated fatty acids they may suffer dermatitis, growth retardation, neurological and visual disturbances.
  • C-20 polyunsaturated fatty acids, belonging to omega-3 and also omega-6 polyunsaturated fatty acid families, are the precursors eicosanoids (prostaglandins, prostacyclin, thromboxanes, and leukotrienes), potent, short-acting, local hormones.
  • While the omission in the diet of omega-6 polyunsaturated fatty acids results in a manifest systemic dysfunction, the deprivation of omega-3 polyunsaturated fatty acids causes dysfunction in a wide range of behavioral and physiological modalities.
References

Akoh C.C. and Min D.B. “Food lipids: chemistry, nutrition, and biotechnology” 3th ed. 2008

Aron H. Uber den Nahvert (On the nutritional value). Biochem Z. 1918;92:211–233 (German)

Bender D.A. “Benders’ dictionary of nutrition and food technology”. 2006, 8th Edition. Woodhead Publishing. Oxford

Bergstroem S., Danielsson H., Klenberg D. and Samuelsson B. The enzymatic conversion of essential fatty acids into prostaglandins. J Biol Chem 1964;239:PC4006-PC4008.

Burr G. and Burr M. A new deficiency disease produced by the rigid exclusion of fat from the diet. J Biol Chem 1929;82:345-67.

Chow Ching K. “Fatty acids in foods and their health implication” 3th ed. 2008

Cozzani I. e Dainese E. “Biochimica degli alimenti e della nutrizione”. Piccin Editore, 2006

Mahan L.K., Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Rosenthal M.D., Glew R.H. Mediacal biochemistry. Human metabolism in health and disease. John Wiley & Sons, Inc. 2009

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

Van D., Beerthuis R.K., Nugteren D.H. and Vonkeman H. Enzymatic conversion of all-cis-polyunsaturated fatty acids into prostaglandins. Nature 1964;203:839-41

Essential fatty acids

Essential fatty acids or EFA are fatty acids which cannot be synthesized de novo by animals, but by plants and microorganisms, such as bacteria, fungi and molds, and whose deficiency can be reversed by dietary addition.
There are two essential fatty acids: linoleic acid or LA (18:2n-6) and α-linolenic acid or ALA (18:3n-3), polyunsaturated fatty acids (PUFAs) with 18 carbon atoms, belonging to omega-6 and omega-3 families, respectively.

Essential Fatty Acids
Fig. 1 – EFA

Animals cannot synthesize these two fatty acids because they lack desaturases that introduce double bonds beyond the Δ9 position (carbon atoms numbered from the methyl end), namely:

  • Δ12-desaturase (E.C. 1.14.19.6), which catalyzes the synthesis of LA from oleic acid;
  • Δ15-desaturase (EC 1.14.19.25), present also in phytoplankton, which catalyzes the synthesis of ALA from linoleic acid.

Essential Fatty AcidsInstead, animals have the enzymes needed to elongate and desaturate, though with low efficiency, the two EFA to form PUFAs with 20, 22, or 24 carbon atoms and up to 6 double bonds, such as for example  dihomo-gamma-linolenic acid or DGLA (20:3n6), arachidonic acid or AA (20:4n6), eicosapentaenoic acid (EPA, 20:5n3), and docosahexaenoic acid or DHA (22:6n3).
If diet is deficient in EFA, also fatty acids synthesized from them become essential. For this reason they may be termed conditionally essential fatty acids.
It should be noted that all essential fatty acids are polyunsaturated molecules but not all polyunsaturated fatty acids are essential, such as those belonging to the omega-7 and omega-9 families.

CONTENTS

Functions of EFA and their PUFA derivatives

The first evidence of their existence dates back to 1918, when Hans Aron suggested that dietary fat could be essential for the healthy growth of animals and that, besides its caloric contribution, there was a inherent nutritive value deriving from the presence of certain lipid molecules
In 1927, Herbert M. Evans and George Oswald Burr demonstrated that, despite the addition of vitamins A, D, and E to the diet, a deficiency of fat severely affected both growth and reproduction of experimental animals. Therefore, they suggested the presence in the fat of an essential substance they called vitamin F.

Essential Fatty Acids
Fig. 2 – Docosahexaenoic Acid

Eleven years after Aron work, in 1929, George Burr and his wife Mildred developed the hypothesis that warm-blooded animals were not able to synthesize appreciable amounts of certain fatty acids. One year later, they discovered that linoleic acid was essential for animals, and it was they who coined the term essential fatty acid.
However, EFA deficiency in humans was first described only in 1958, in infants fed a milk-based formula lacking them.
And in 1964, thanks to the research by Van Dorp et al. and Bergstroem et al., one of their biological functions, that is, being precursor for the synthesis of prostaglandins, was discovered.
Now, it is clear that EFA and derived PUFAs play many important roles, some of which are listed below.

  • They are fundamental components of biological membranes, modulating, for example, their fluidity, particularly DHA.
  • They are essential for the proper development and functioning of the nervous system, particularly AA and DHA.
  • They are involved in membrane signal transduction, particularly omega-6 fatty acids, such as membrane phospholipid arachidonic acid.
  • They are involved in the regulation of genes encoding lipolytic and lipogenic enzymes. In fact they are strong inducers of  fatty acid oxidation, as well as inhibitors of their synthesis and that of triglycerides, at least in animal models, by acting, for example, as:

activators of the peroxisome proliferator-activated receptor α or PPAR-α, which stimulates, among other things, the transcription of genes encoding lipolytic enzymes as well as mitochondrial and peroxisomal β-oxidation enzymes, and inhibits the transcription of genes encoding for enzymes involved in lipogenesis;

inhibitors of sterol responsive element binding protein-1c (SREBP-1c) gene transcription, a hepatic transcription factor required for liver fatty acid and triglyceride synthesis induced by insulin.
Note: PUFA also increase SREBP 1c mRNA degradation as well as SREBP-1 protein degradation.

  • They are precursors of signaling molecules, with autocrine and paracrine action, which act as mediators in many cellular processes. Eicosanoids, a group of oxygenated, 20 carbon fatty acids, are probably the most studied. They derive from linoleic acid, dihomo-gamma-linolenic acid, arachidonic acid, and EPA, and include prostaglandins, thromboxanes, leukotrienes, lipoxins, and  epoxyeicosatrienoic acids.
  • They are essential, especially LA present in sphingolipids of the stratum corneum of the skin, for the formation of the barrier against water loss from the skin itself.
  • They have a crucial role in the prevention of many diseases, particularly coronary heart disease or CHD, acting as antihypertensive, antithrombotic, and triglyceridelowering agents (increasing in the latter case mitochondrial β-oxidation).
  • Finally, energy storage function is marginal.

Foods rich in essential fatty acids and derived PUFAs

Linoleic acid, produced mainly by terrestrial plants, is the most abundant polyunsaturated fatty acid in the Western diet, and accounts for 85-90% of dietary omega-6 fatty acids.
In the human diet, the richest sources are vegetable oils and seeds of many plants, such as:

  • safflower oil, ~ 740 mg/g
  • sunflower oil, ~ 600 mg/g
  • soybean oil, ~ 530 mg/g
  • corn oil, ~ 500 mg/g
  • cotton seed oil, ~ 480 mg/g
  • walnuts, ~ 340 mg/g
  • brazil nuts, ~ 250 mg/g
  • peanut oil, ~ 240 mg/100 g
  • canola oil, ~ 190 mg/g
  • peanuts, ~140 mg/g
  • flaxseed oil, ~ 135 mg/g

Linoleic acid is present in fair amount also in animal products such as chicken eggs or lard, but only because it is present in their feed.
It should be noted that some of the major sources of LA such as walnuts, flax seed oil, soybean oil, and canola oil are also rich sources of α-linolenic acid (see below).
In seed oils, omega-6 fatty acids with a chain length longer than 18 carbon atoms, such as DGLA and arachidonic acid, are present only in traces. Instead, AA is found in all animal tissues and animal-based foods.

α-Linolenic acid is produced by plants, also cold water vegetation such as algae and phytoplankton.
In the human diet, some of the richest sources are:

  • flax seed oil, ~ 550 mg/g
  • rapeseed oil, ~ 85 mg/g
  • soybean oil, ~ 75 mg/g

Other foods rich in ALA are nuts, ~ 70 mg/g, and soybeans, ~ 10 mg/g.
EPA and DHA are mainly found in marine algae, and in engineered algae DHA can represent about 50% of the total fatty acids. In the human diet, EPA and DHA derive from fish, shellfish and fish oil, particularly that derived from cold-water fatty fish.

Essential fatty acids in Western diets

Over the past 50 years, Western diet has been enriched in saturated fatty acids and omega-6 fatty acids, whereas has become poor  in omega-3 fatty acids, with an omega-6/omega-3 ratio between 10/1 and 20/1, and hence, far from the recommended ratio of 5:1.
This high ratio is due to several factors, some of which are listed below.

  • While wild plant foods are typically high in omega-3 fatty acids, in industrial agriculture crops rich in omega-6 fatty acids have had greater success than those rich in omega-3 fatty acids.
  • The low consumption of seafood and fish oil.
  • The high consumption of animal products derived from animals, such as chickens, cattle and pigs, raised on corn-based feed. In addition to this, omega-3 fatty acid content, of some species of farmed fish is lower than their wild counterparts, again because of the feed used.
  • The high consumption of vegetable oils low in omega-3 fatty acids and high in omega-6 fatty acids, such as safflower oil, sunflower oil, soybean oil and corn oil.
  • The increased shelf life of those foods in which omega-6 fatty acids predominate over omega-3-fatty acids.

So, although it is desirable to increase consumption of omega-3 fatty acids, this will not occur easily.

Omega-6/omega-3 ratio

Many evidences, like lower rates of incidence of cancer, autoimmunity and coronary heart disease in populations whose diet has a high ratio of omega-3 to omega-6 fatty acids, such as Eskimos, Japanese and others who consume a large amount of seafood, suggest that the change of this ratio has affected human physiology adversely, promoting, together with other factors such as smoking and a sedentary lifestyle, the development of the main classes of diseases.
Note: Japanese are the only people with an omega-3/omega-6 ratio of 1/2-4.

Recommended dietary intake

Hereinafter, the recommended dietary intake for omega-3 and omega-6 fatty acids for healthy adults, according to the recommendation of some of the major scientific societies and international organizations, and, as you will see, there is no common position.

  • Omega-3 fatty acids
    WHO recommends a dietary intake of omega-3-fatty acids between 0.5 and 2% of energy/day, with 300-500 mg of EPA/DHA per day, and 0.8-1.1 g per day of α-linolenic acid.
    Academy of Nutrition and Dietetics recommends a dietary intake of 500 mg of EPA/DHA per day.
    European Food Safety recommends a dietary intake of 250 mg of EPA/DHA per day.
    American Heart Association and American Diabetes Association recommend to eat fish at least twice a week, particularly fatty fish.
    American Heart Association recommends to include oils and foods rich in α-linolenic acid.
  • Omega-6 fatty acids
    In the past, dietary recommendations for omega-6 fatty acid intakes, and so especially linoleic acid, were focused on the prevention of their deficiency, while currently they are focused on the determination of the optimal intake to reduce the risk of chronic diseases, with special attention to CHD.
    Currently, most scientific societies recommend a daily intake of linoleic acid between 5 and 10% of energy/day. This daily intake seems able to reduce the risk of CHD and coronary heart disease deaths compared to lower intakes.

References

Akoh C.C. and Min D.B. “Food lipids: chemistry, nutrition, and biotechnology” 3th ed. 2008

Bergstroem S., Danielsson H., Klenberg D. and Samuelsson B. The enzymatic conversion of essential fatty acids into prostaglandins. J Biol Chem 1964;239:PC4006-PC4008.

Burr G. and Burr M. A new deficiency disease produced by the rigid exclusion of fat from the diet. J Biol Chem 1929;82:345-67.

Chow Ching K. “Fatty acids in foods and their health implication” 3th ed. 2008

De Meester F., Watson R.R.,Zibadi S. Omega-6/3 fatty acids: functions, sustainability strategies and perspectives. Springer Science & Business Media, 2012 [Google eBook]

Evans H. M. and G. O. Burr. A new dietary deficiency with highly purified diets. III. The beneficial effect of fat in the diet. Proc Soc Exp Biol Med 1928;25:390-7. doi:10.3181/00379727-25-3867

FAO. Global Recommendations for EPA and DHA Intake (As of 30 June 2014).

Harris W.S., Mozaffarian D., Rimm E.B., Kris-Etherton P.M., Rudel L.L., Appel L.J., Engler M.M., Engler M.B., Sacks F.M. Omega-6 fatty acids and risk for cardiovascular disease. Circulation 2009;119:902-7. doi:10.1161/CIRCULATIONAHA.108.191627

Rosenthal M.D., Glew R.H. Mediacal biochemistry. Human metabolism in health and disease. John Wiley & Sons, Inc. 2009

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

Simopoulos A.P. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med 2008;233(6):674-88. doi:10.1016/S0753-3322(02)00253-6

Van Dorp. D.A., Beerthuis R.K., Nugteren D.H. and Vonkeman H. Enzymatic conversion of all-cis-polyunsaturated fatty acids into prostaglandins. Nature 1964;203:839-41. doi:10.1038/203839a0

Vannice G., Rasmussen H. Position of the academy of nutrition and dietetics: dietary fatty acids for healthy adults. J Acad Nutr Diet. 2014;114(1):136-53. doi:10.1016/j.jand.2013.11.001

Nutrition for athletes: strategies for training and competition

Nutrition for Athletes
Fig. 1 – Fruit and Vegetables

The right diet is one of the basic foundations for achieving the best athletic performance.
Unfortunately, there aren’t special diets or “magic” foods.
Athletes, as the rest of the population, should follow a Mediterranean-type diet, so providing an adequate intake of energy, of mineral salts, vitamins, antioxidants, fiber and water, keeping at the same time  good  balance  of caloric intake by wisely splitting it during the day.
Finally, they should avoid as much as possible industrial foods or fast foods.

Nutrition for athletes and the distribution of meals and calories

Still more than sedentary man, because of his greater caloric intake, athlete will have to consume more meals during the day to avoid concentrating an excessive amount of calories (and food) in one meal.
In this way, he will:

  • avoid reaching lunch-time and especially dinner-time with an excessive hunger;
  • digest foods more easily, not engaging the digestive system with too much abundant meals.
  • avoid any increases in blood chemistry parameters associated with an increased risk of cardiovascular disease, such as hypertriglyceridemia and hypercholesterolemia.

Of course, in nutrition for athletes, the distribution of the meals will have to consider also training and competition times. The best distribution might be: breakfast, lunch and dinner plus two snacks, one in the morning and the other in the afternoon.

Breakfast

Nutrition for Athletes
Fig. 2 – Glass of Milk

It is of one of most important and often underestimated meals of the day, that should never be skipped.
Typical breakfast foods are milk and/or yogurt, fruit juice (better if freshly squeezed seasonal fruit; when you buy a packaged fruit juice, select it without added sugar/sweeteners and with a caloric content of about 45 kcal/100 g), freshly made tea,bread, dry cookies without cream (however moderately), corn flakes without addition of syrup, honey, fresh/dry fruit, chocolate, and jam/honey (the last three in moderation).
Breakfast will be consumed considering the time when physical activity, and still more the competition, is made.
In nutrition for athletes, as for sedentary population,the breakfast should represent about 15% of the daily caloric intake, to pass to 20% without mid-morning snack.

Lunch

It should represent the meal in which the major part of complex carbohydrates is taken up that is pasta, rice, barley, cous-cous, oats, millet, etc (better if “al dente” with a light seasoning), based on personal preferences.
To limit glycemic increase it is advisable to eat, after a dish rich in carbohydrates, vegetables, fresh or cooked (in the latter when possible, better if steamed), but avoiding potatoes, cooked carrots and onions (foods with an high glycemic index). Bread, if present, should be eaten moderately.
At the end of the lunch a fruit can be eaten as well (if it doesn’t cause feelings of bloating when eaten at the end of the meal; in the case, fruit may be eaten during snacks) and/or a dessert without cream.
Seasonal fruit and vegetable will ensure an adequate intake of mineral salts, vitamins, fiber and water.
It is advisable having lunch at least two-three hours before the start of training sessions/competition, in order to allow a complete digestion, normalization of postprandial glycemic peaks and of insulin response before starting workout.
In nutrition for athletes, the lunch should represent 25-30% of the daily caloric intake.

Dinner

In this meal, it is advisable to give priority to proteins rather than carbohydrates, hence fish, white or red meat (the last one lean and less frequently) or legumes (rich in slow absorption carbohydrates, fiber and mineral salts) will be present, with seasonal vegetables, fresh or cooked, (recommended is also a vegetable soup, that will help in restoring liquids), moderate bread, and fruit (if it doesn’t cause feelings of bloating when eaten at the end of the meal, as seen for lunch).
It is advisable to eat legumes at dinner to avoid bothersome bloating during training.
In nutrition for athletes, the dinner should represent 25-30% of the daily caloric intake.

Snacks

In nutrition for athletes, to ensure adequate distribution of calories, often much higher than in the sedentary man and avoid an excessive accumulation at major meals, at least two snacks must be present, one at mid-morning and the other at mid-afternoon. Assume preferably fruit (moderately also dry fruit, advisable walnuts and almonds), yogurt/milk, dry cookies or a sandwich with lean sliced salami (e.g. lean raw ham or cured raw beef), cottage cheese (soft fresh cheese) or simply with extra-virgin olive oil and tomato or other vegetables (always choose seasonal vegetables).
The snack should represent 10-15% of the daily caloric intake.

Daily caloric intake

In nutrition for athletes, caloric intake must be matched to energy consumption that, in turn, depends on:

  • sex;
  • age;
  • growing phase;
  • physical structure;
  • level of physical activity (training plane, competition, recovery);
  • even possible pathological states.

Athlete’s diet must consider energy consumption due to workload sustained during training sessions.
In fact, if there are sports (as swimming, running, rowing or cross-country skiing) whose training sessions cause an increase of energy requirement in excess of 50% compared to needs referred to a moderately active lifestyle, in other sports (as artistic or rhythmic gymnastics, shooting etc.) the consumption related to the activity may be modest.
So, the only difference in nourishment between a sedentary or moderately active man and an athlete engaged in sports causing a large increase of energy requirement will be of quantitative type: the greater is the energy expenditure linked to physical activity, the greater will be the caloric intake.

References

Giampietro M. L’alimentazione per l’esercizio fisico e lo sport. Il Pensiero Scientifico Editore. Prima edizione 2005

Jeukendrup A.E. Nutrition for endurance sports: marathon, triathlon, and road cycling. J Sport Sci 2011:29;sup1, S91-S99. doi:10.1080/02640414.2011.610348

Mahan L.K., Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Shils M.E., Olson J.A., Shike M., Ross A.C.: “Modern nutrition in health and disease” 9th ed. 1999

Yo-yo effect or weight cycling

What is yo-yo effect?

Weight cycling or yo-yo effect, i.e. repeated phases of loss and weight gain, appears related to excess weight and accumulation of fat in the abdomen.

Yo-yo effect and health

Several studies suggest a link with increased blood pressure, increased blood cholesterol, with gallbladder disease, with a significant increase in binge eating disorder, in women with greater easy to weight gain than those who are not subject to weight cycling. In this regard there should be emphasized that the weight cycling occurs over years, during which, aging, the rate of metabolism inevitably tends to decrease: this could make more difficult the subsequent losses.
Finally, weight cycling was also associated with a sense of depression with regard to weight.

References

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:10.1016/j.clnu.2011.06.009

Montani J-P., Viecelli A.K., Prévot A. & Dulloo A.G. Weight cycling during growth and beyond as a risk factor for later cardiovascular diseases: the ‘repeated overshoot’ theory. Int J Obes (Lond) 2006;30:S58-S66. doi:10.1038/sj.ijo.0803520

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:10.1161/hc4001.096152

Invert sugar: definition, production, uses

Invert sugar (also known as inverted sugar) is sucrose partially or totally cleaved into fructose and glucose (also known dextrose) and, apart from the chemical process used (see below), the obtained solution has the same amount of the two monosaccharides.
Moreover, according to the product, not cleaved sucrose may also be present.

Invert sugar production

The breakdown of sucrose may happen in a reaction catalyzed by enzymes, such as:

  • sucrase, active at our own intestinal level;
  • invertase, an enzyme secreted by honeybees into the honey and used industrially to obtain invert sugar.

Another process applies acid action, as it happens partly in our own stomach and as it happened in the old times, and still happens, at home-made and industrial level. Sulfuric and hydrochloric acids was used, heating the solution with caution for some time; in fact the reaction is as fast as the solution is acid, regardless of the type of acid used, and as higher the temperature is. The acidity is then reduced or neutralized with alkaline substances, as soda or sodium bicarbonate.

A chemical process as described occurs when acid foods are prepared; i.e. in the preparation of jams and marmalades, where both conditions of acidity, naturally, and high temperatures, by heating, are present. The situation is analogous when fruit juices are sweetened with sucrose.
The reaction develops at room temperature as well, obviously more slowly.
What is the practical outcome of that?
It means that, during storage, also sweets and acid foods, even those just seen, go towards a slow reaction of inversion of contained/residue sucrose, with consequent modification of the sweetness, since invert sugar at low temperatures is sweeter (due to the presence of fructose), and assumption of a different taste profile.

Properties and uses

It is principally utilized in confectionery and ice-cream industries thanks to some peculiar characteristics.

  • It has an higher affinity for water (hydrophilicity) than sucrose (see fructose) therefore it keeps food more humid: e.g. cakes made with invert sugar dry up less easily.
  • It avoids or slows down crystal formation (dextrose and fructose form less crystals than sucrose), property useful in confectionery industries for icings and coverage.
  • It has a lower freezing point.
  • It increases, just a bit, the sweetness of the product in which it has been added, as it is sweeter than an equal amount of sucrose (the sweetness of fructose depends on the temperature in which it is present).
  • It may take part to Maillard reaction (sucrose can’t do it) thus contributing to the color and taste of several bakery products.

It should be noted that honey, lacking in sucrose, has almost the same composition in fructose and glucose of the 100% invert sugar (fructose is slightly more abundant than glucose). So, diluted honey, better if not much aromatic, may replace industrial invert sugar.

References

Belitz .H.-D., Grosch W., Schieberle P. “Food Chemistry” 4th ed. Springer, 2009

Bender D.A. “Benders’ Dictionary of Nutrition and Food Technology”. 8th Edition. Woodhead Publishing. Oxford, 2006

Bressanini-lescienze.blogautore.espresso.repubblica.it

Mahan LK, Escott-Stump S.: “Krause’s foods, nutrition, and diet therapy” 10th ed. 2000

Shils M.E., Olson J.A., Shike M., Ross A.C. “Modern nutrition in health and disease” 9th ed., by Lippincott, Williams & Wilkins, 1999

Stipanuk M.H., Caudill M.A. Biochemical, physiological, and molecular aspects of human nutrition. 3rd Edition. Elsevier health sciences, 2013 [Google eBooks]

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