Category Archives: Nutrition

Nutrition is a key factor in maintaining good health throughout life.
Eating a balance diet, from birth with breastfeeding, and later during childhood, adolescence and adult life, is helpful in achieving and maintaining a good state of health and contributes, when associated with a healthy lifestyle, to the prevention of many chronic diseases such as cardiovascular diseases, osteoporosis, type II diabetes, and many types of cancers, conditions which are increasingly common nowadays.
And it is important to point out the relationship between nutrition and the intestinal microbiota, the community of microorganisms that colonize the gut: diet seems to be main factor in determining its composition, starting from breast milk.
Proper nutrition is essential even in the presence of allergic reactions to food components, as in the case of celiac disease, condition in which all food containing gluten must be avoided for life.
Proper nutrition is essential for athletes, and when combined with adequate training improves the performance in any sports.
And among the different types of diets, the Mediterranean diet is one of the healthiest. This dietary pattern was brought to the attention of the international scientific community in the 1950s by the work of Ancel Keys, an American physiologist. The Mediterranean diet, rich in plant products, such as extra virgin olive oil, vegetables, legumes, and whole grains, and low in red meats and derived products and high fat dairy products, ensures an good supply of fiber, compounds with anti-inflammatory and antioxidant actions, as well as a low intake of saturated fats.

Blood pressure, hypertension and dietary sodium

A high sodium (Na+) intake (the main source is salt or sodium chloride NaCl) contributes to blood pressure raise, and hypertension development.
Many epidemiologic studies, animal studies, migration studies, clinical trials, and meta-analyses of trials support this, with the final evidence from rigorously controlled, dose-response trials. Furthermore, in primitive society Na+ intake is very low and people experience very low hypertension, and the blood pressure increase with age does not occur.
Probably, sodium intake effect sizes are to be underestimated!

CONTENTS

Recommended daily intake

Sodium’s physiologic requires are very low; in fact, the minimum recommended Na+ intake for maintain life is 250 mg/day (Note: iodized salt is an important source of dietary iodine in the United States and worldwide).
An Americans consumes the mineral in great excess of physiologic requires: despite the guidelines from the Departments of Agriculture and Health and Human Services, during the period from 2005 through 2006 the average salt intake in USA is of 10.4 g/day for the average man and 7.3 for the average woman, amount in excess regarding preceding years.
A study published on February 2010 on “The New England Journal of Medicine” have shown that “A population-wide reduction in dietary salt of 3 g per day (1200 mg of Na+ per day) is projected to reduce the annual number of new cases of coronary heart disease (CHD) by 60,000 to 120,000, stroke by 32,000 to 66,000, and myocardial infarction by 54,000 to 99,000 and to reduce the annual number of deaths from any cause by 44,000 to 92,000″ (Bibbins-Domingo et all., see References). These benefits are similar in magnitude to those from:

  • a 50% reduction in tobacco use;
  • a 5% reduction in body mass index among obese adults;
  • a reduction in cholesterol levels.

These benefits regard all adult group age, black and nonblack, male and female. The benefits for black are greater than nonblack, in both sex and all age group. It’s estimated an annual savings of $10 billion to 24 $ billion in health care costs.
Clinical trials have also documented that a reduced Na+ intake can lower blood pressure in the setting of antihypertensive medication, and can facilitate hypertension control.
But, in USA dietary salt intake is on the rise!
So, it is recommended, to prevent hypertension development, a reduction in its intake and, in view of the available food supply and the currently daily Na+ intake, a reasonable recommendation is an upper limit of 2.3 g/day (5.8 g/day of salt).
How achieves this level? It can be achieved:

  • cooking with as little salt as possible;
  • refraining from adding salt at the table;
  • avoiding highly salted, processed foods.

Food sources of sodium

They include:

  • salt used at the table: up to 20% of the daily salt intake;
  • salt or sodium compounds added during preparation or processing foods: between 35 to 80% of the daily sodium intake comes from processed foods.A major source of sodium is salt, or sodium chlorideWhich foods are?
    Processed, smoked or cured meat and fish e.g. sliced salami, sausage, salt pork, tuna fish in oil etc.; meat extracts and sauce, salted snack, soy sauce, barbecue sauce, commercial salad dressing; prepackage frozen foods; canned soup, canned legumes; cheese etc.
    There are also many sodium-containing additives as disodium phosphate (e.g. in cereals, ice cream, cheese), monosodium glutamate (i.e. meat, soup, condiments), sodium alginate (e.g. in ice creams), sodium benzoate (e.g. in fruit juice), sodium hydroxide (e.g. in pretzels, cocoa product), sodium propionate (e.g. in bread), sodium sulfite (e.g. in dried fruit), sodium pectinate (e.g. syrups, ice creams, jam), sodium caseinate (e.g. ice creams and other frozen products) and sodium bicarbonate (e.g. baking powder, tomato soup, confections).
    So pay attention to ingredients!
  • Inherent sodium of foods. Generally low in fresh foods.

The blood pressure response to lower dietary Na+ intake is heterogeneous with individuals having greater or lesser degrees of blood pressure reduction. Usually the effect of reduction tend to be greater in blacks, middle-aged and older persons, and individuals with hypertension, diabetes or chronic kidney disease.
Furthermore genetic and dietary factors influence the response to sodium reduction.

Diet modifies response of blood pressure to sodium

Some components of the diet may modify response of blood pressure to sodium.

  • A high dietary intake of calcium and potassium rich foods, such as fruit, vegetable, legumes (e.g. Mediterranean diet), and low-fat dairy products (e.g. DASH diet), may prevent or attenuate the rise in blood pressure for a given increase in sodium intake.
  • Some evidences, seen primarily in animal model, suggest that high dietary intake of sucrose may potentiate salt sensitivity of blood pressure.

Note: high Na+ intake can contribute to osteoporosis: they result in an increase in renal calcium excretion, particularly if daily calcium intakes are low.

References

Appel L.J., Brands M.W., Daniels S.R., Karanja N., Elmer P.J. and Sacks F.M. Dietary approaches to prevent and treat HTN: a scientific statement from the American Heart Association. Hypertension 2006;47:296-308. doi:10.1161/01.HYP.0000202568.01167.B6

Bibbins-Domingo K., Chertow G.M., Coxson P.G., Moran A., Lightwood J.M., Pletcher M.J., and Goldman L. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med 2010;362:590-599. doi:10.1056/NEJMoa0907355

Cappuccio FP. Overview and evaluation of national policies, dietary recommendtions and programmes around the world aiming at reducing salt intake in the population. World Health Organization. Reducing salt intake in populations: report of a WHO forum and technical meeting. WHO Geneva 2007;1-60.

Chen J, Gu D., Jaquish C.E., Chen C., Rao D.C., Liu D., Hixson J.E., Lee Hamm L., Gu C.C., Whelton P.K. and He J. for the GenSalt Collaborative Research Group. Association Between Blood Pressure Responses to the Cold Pressor Test and Dietary Sodium Intervention in a Chinese Population. Arch Intern Med. 2008;168:1740-1746. doi:10.1001/archinte.168.16.1740

Denton D.,  Weisinger R., Mundy N.I., Wickings E.J., Dixson A., Moisson P., Pingard A.M., Shade R., Carey D., Ardaillou R., Paillard F., Chapman J., Thillet J. & Michel J.B. The effect of increased salt intake on blood pressure of chimpanzees. Nature Med 1995;10:1009-1016. doi:10.1038/nm1095-1009

Ford E.S., Ajani U.A., Croft J.B., Critchley J.A., Labarthe D.R., Kottke T.E., Giles W.H, and Capewell S. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. N Engl J Med 2007;356:2388-2398. doi:10.1056/NEJMsa053935

Geleijnse J.M., Witteman J.C., den Breeijen J.H., Hofman A., de Jong P., Pols H.A. and Grobbee D.E. Dietary electrolyte intake and blood pressure in older subjects: the Rotterdam Study. J Hyperten 1996;14:73741.

Harlan W.R. and Harlan L.C. Blood pressure and calcium and magnesium intake. In: Laragh J.H., Brenner B.M., eds. Hypertension: pathophysiology, diagnosis and management. 2end ed. New York: Raven Press 1995;1143-1154

Holmes E., Loo R.L., Stamler J., Bictash M., Yap I.K.S., Chan Q., Ebbels T., De Iorio M., Brown I.J., Veselkov K.A., Daviglus M.L., Kesteloot H., Ueshima H., Zhao L., Nicholson J.K. and Elliott P. Human metabolic phenotype diversity and its association with diet and blood pressure. Nature 2008;453:396-400. doi:10.1038/nature06882

Pickering T.G. New guidelines on diet and blood pressure. Hypertension 2006;47:135-136. doi:10.1161/01.HYP.0000202417.57909.26

Simpson F.O. Blood pressure and sodium intake. In: Laragh J.H., Brenner B.M. eds. Hypertension: pathophysiology, diagnosis and management. 2end ed. New York: Raven Press 1995;273-281

Strazzullo P., D’Elia L., Kandala N. and Cappuccio F.P. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ 2009;339:b4567. doi:10.1136/bmj.b4567

Tzoulaki I., Brown I.J., Chan Q., Van Horn L., Ueshima H., Zhao L., Stamler J., Elliott P., for the International Collaborative Research Group on Macro-/Micronutrients and Blood Pressure. Relation of iron and red meat intake to blood pressure: cross sectional epidemiological study. BMJ 2008;337:a258. doi:10.1136/bmj.a258

Weinberger M.H. The effects of sodium on blood pressure in humans. In: Laragh JH, Brenner BM, eds. Hypertension: pathophysiology, diagnosis and management. 2end ed. New York: Raven Press 1995;2703-2714.

Writing Group of the PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER Clinical Trial. JAMA 2003;289:2083-2093. doi:10.1001/jama.289.16.2083

World Health Organization, International Society of Hypertension Writing Group. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. Guidelines and recommendations. J Hyperten 2003;21:1983-1992.

Human health and carotenoids

Carotenoids belong to the category of bioactive compounds taken up with diet, that is, molecules able to provide protection against many diseases such as cardiovascular diseases, cancer and macular degeneration. They are also important for the proper functioning of the immune system.
Among the mechanisms that seem to be at the basis of their human health-promoting effects have been reported (Olson, 1999, see References):

  • the capability to quench singlet oxygen (see above);
  • the scavenging of peroxyl radicals and reactive nitrogen species;
  • the modulation of carcinogen metabolism;
  • the inhibition of cell proliferation;
  • the enhancement of the immune response;
  • a filtering action of blue light;
  • the enhancement of cell differentiation;
  • stimulation of cell-to-cell communication

Carotenoids and antioxidant activity

Carotenoids, with the adaptation of organisms to aerobic environment, and therefore to the presence of oxygen, have offered protection against oxidative damage from free radicals, particularly by singlet oxygen, a powerful oxidizing agent (see also below).
Carotenoids stabilize singlet oxygen acting both chemical and physical point of view:

  • chemical action involves the union between the two molecules;
  • in physical action, the radical transfers its excitation energy to the carotenoid. The result is a low energy free radical and an excited carotenoid; later, the energy acquired by the carotenoid is released as heat to the environment, and the molecule, that remains intact, is ready to carry out another cycle of stabilization of singlet oxygen, and so on.
Human health and carotenoids
Fig. 1 – Free Radical

The capability of carotenoids to quench singlet oxygen is due to the conjugated double-bond system present in the molecule, and the maximum protection is given by those molecules that have nine or more double bonds (moreover, the presence of oxygen in the molecule, as in xanthophylls, seems to have a role).
Carotenoids are involved not only in singlet oxygen quenching, but also in the scavenging of other reactive species both of oxygen, as peroxyl radicals (therefore contributing to the reduction of lipid peroxidation) and nitrogen. These reactive molecules are generated during the aerobic metabolism but also in the pathological processes.

Lycopene, xanthophylls and human health

Lycopene, a carotene, canthaxanthin and astaxanthin, two xanthophylls present in foods of animal origin, are better antioxidants than beta-carotene but also than zeaxanthin that, with lutein, is involved in prevention of age-related macular degeneration.
Lycopene, in addition to act on oxygen free radicals, acts as antioxidant also on the radicals of vitamin C and vitamin E, that are generated during the antioxidant processes in which these vitamins are involved, “repairing them”.
Finally, lycopene exerts its antioxidant action also indirectly, inducing the synthesis of enzymes involved in the protection against the action of oxygen free radicals and other electrophilic species; these enzymes are quinone reductase, glutathione S-transferase and superoxide dismutase (they are part of the enzymatic antioxidant system).

Vitamin A and human health

Vitamin A, whose deficiency affects annually more than 100 million children worldwide, causing more than a million deaths and half million cases of blindness, is a well-known carotenoid derivative with many biological actions, being essential for reproduction, growth, vision, immune function and general human health.
In the human diet, the major sources of vitamin A are the preformed vitamin, which is found in foods of animal origins (meat, milk, eggs, etc), and provitamin A carotenoids, present in fruits and vegetables. In economically deprived countries, fruits and vegetables are the main source of vitamin A being less expensive than food of animal origin.
Of the more than 750 different carotenoids identified in natural sources, only about 50 have provitamin A activity, and among these, beta-carotene (precisely, all-trans-beta-carotene isomer) is the main precursor of the vitamin A.
Among the other carotenoids precursors of vitamin A, alpha-carotene, gamma-carotene, beta-cryptoxanthin, alpha-cryptoxanthin, and beta-carotene-5,6-epoxide have about half the bioactivity of beta-carotene.

Human health and vitamin A
Fig. 2 – Provitamin A Activity

Spinach, carrots, pumpkins, sweet potatoes (yellow) are example of vegetables rich in beta-carotene and other provitamin A carotenoids.
Acyclic carotenes, such as lycopene (the main carotenoid in the human diet), and xanthophylls, except those mentioned above (beta-cryptoxanthin, alpha-cryptoxanthin, and beta-carotene-5,6-epoxide), cannot be converted to vitamin A.

References

de la Rosa L.A., Alvarez-Parrilla E., Gonzàlez-Aguilar G.A. Fruit and vegetable phytochemicals: chemistry, nutritional value, and stability. 1th Edition. Wiley J. & Sons, Inc., Publication, 2010

Johnson E.J. The role of carotenoids in human health. Nutr Clin Care 2002;5(2):56-65. doi:10.1046/j.1523-5408.2002.00004.x

Olson, J.A. 1999. Carotenoids. p. 525-541. In: Shils M.E., Olson J.A., Shike M., Ross A.C. “Modern nutrition in health and disease” 9th ed., by Lippincott, Williams & Wilkins, 1999

Ross A.B., Thuy Vuong L., Ruckle J., Synal H.A., Schulze-König T., Wertz K., Rümbeli R., Liberman R.G., Skipper P.L., Tannenbaum S.R., Bourgeois A., Guy P.A., Enslen M., Nielsen I.L.F., Kochhar S., Richelle M., Fay L.B., and Williamson G. Lycopene bioavailability and metabolism in humans: an accelerator mass spectrometry study. Am J Clin Nutr 2011;93:1263-1273. doi:10.3945/ajcn.110.008375

Role of carotenoids in plants and foods

Through the course of evolution, carotenoids, thank to their unique physical and chemical properties, have proven to be highly versatile molecules, being able to perform many functions in many different organisms, like plants.

Carotenoids in photosynthesis

Carotenoids, in the early stages of the emergence of single-celled photosynthetic organisms, are probably been used for light harvesting at wavelengths different from those covered by chlorophyll. Therefore carotenoids, acting as light absorbing accessory pigments, have allowed to expand the range of solar radiation absorbed and so utilized for photosynthesis, energy that is then transferred to chlorophyll itself.
The major carotenoids involved in light harvesting, that accumulate in green plant tissues, are beta-carotene, lutein, neoxanthin, and violaxanthin, that absorb light energy in the 400- to 500-nm range.
Moreover, they protect chlorophyll from photooxidation (in humans, they may contribute to the protection of photo-oxidative damage caused by UV rays, thus acting as a endogenous photo-protective agents).

Carotenoids and autumn leaf color

Leaf color of deciduous plants in different seasons, green, yellow, orange or red, is due to the presence in them of natural pigments.
In spring and summer, the predominant pigment present in the leaf is chlorophyll, and therefore the color is green.
Carotenoids and PlantsDuring the fall, the color changes from green to yellow, orange or red, depending on the type of plant: this is a consequence of the change, both qualitative and quantitative, in the pigment content.
In fact, as a result of the decrease of the temperature and daylight hours, the production of chlorophyll is interrupted and that already present is demolished into colorless metabolites. In this way the predominant pigments become carotenoids (yellow-orange), molecules much more stable than the chlorophyll, which remain in the leaf coloring it (it do not seem to be synthesized de novo), and anthocyanins (red-purple), which, unlike carotenoids, are not present during the growing season, but are synthesized in autumn, just before leaf fall. Therefore, it can be concluded that the red-purple color assumed from the leaves of certain plants is not a side effect of leaf senescence but results from anthocyanins de-novo synthesis.
Depending on the prevalence of carotenoids or anthocyanins, leaf color changes from green to yellow/orange, as in Ginkgo biloba (yellow), or red-purple as in some maples.

And plants with non green leaves?
Their color is not due to the absence of chlorophyll but the presence of very high amounts of other pigments, typically carotenoids and anthocyanins, that “cover” the chlorophyll, determining the color of the leaf.

Some functions of apocarotenoids in plants and foods

These oxygenated carotenoids, containing fewer than 40 carbon atoms, have many functions in plants and animals and are also important for the aroma and flavor of foods.
Some of their main functions include the following.

  • Apocarotenoids have significant roles in the response signals involved in the development and in the response to the environment (for example abscisic acid).
  • They can act as visual or volatile signals to attract pollinators.
  • They are important in the defense mechanisms of plants.
  • They have a role in regulating plant architecture.
  • An apocarotenal, trans-beta-apo-8′-carotenal, found in citrus fruits and spinach, with a low provitamin A activity, is used in pharmaceuticals and cosmetics, and is also a food additive (E160e) legalized by the European Commission for human consumption.
  • Apocarotenoids make an important contribution to the nutritional quality and flavor of many types of foods such as fruits, wine and tea. Two natural apocarotenoids, crocetin and bixina, have economic importance as they are used as pigments and aroma in foods.
  • Finally, a broad range of apocarotenals derive from oxidative reactions that occur in food processing; these molecules are intermediates in the formation of smaller molecules, important for the color and flavor of the food.

References

Archetti, M., Döring T.F., Hagen S.B., Hughes N.M., Leather S.R., Lee D.W., Lev-Yadun S., Manetas Y., Ougham H.J. Unravelling the evolution of autumn colours: an interdisciplinary approach. Trends Ecol Evol 2009;24(3):166-73. doi:10.1016/j.tree.2008.10.006

de la Rosa L.A., Alvarez-Parrilla E., Gonzàlez-Aguilar G.A. Fruit and vegetable phytochemicals: chemistry, nutritional value, and stability. 1th Edition. Wiley J. & Sons, Inc., Publication, 2010

Maltodextrin, fructose and endurance sports

Carbohydrate ingestion can improve endurance capacity and performance.
The ingestion of different types of carbohydrates, which use different intestinal transporters, can:

  • increase total carbohydrate absorption;
  • increase exogenous carbohydrate oxidation;
  • and therefore improve performance.

Glucose and fructose

When a mixture of glucose and fructose is ingested (in the analyzed literature, respectively 1.2 and 0.6 g/min, ratio 2:1, for total carbohydrate intake rate to 1.8 g/min), there is less competition for intestinal absorption compared with the ingestion of an iso-energetic amount of glucose or fructose,  two different intestinal transporters being involved. Furthermore, fructose absorption is stimulated by the presence of glucose.

This can:

  • contribute to a faster rate of monosaccharide absorption;
  • increase the availability of exogenous carbohydrates in the bloodstream;
  • cause the higher exogenous carbohydrate oxidation rates in fructose plus glucose combination compared to high glucose intake alone.

The combined ingestion of glucose and fructose allows to obtain exogenous carbohydrate oxidation rate around 1,26 g/min, therefore, higher than the rate reported with glucose alone (1g/min), also in high concentration.
The observed difference (+0,26 g/min) can be fully attributed to the oxidation of ingested fructose.

Sucrose and glucose

The ingestion of sucrose and glucose, in the same conditions of the ingestion of glucose and fructose (therefore, respectively 1.2 and 0.6 g/min, ratio 2:1, for total carbohydrate intake rate to 1.8 g/min), gives similar results.

Glucose, sucrose and fructose

Very high oxidation rates are found with a mixture of glucose, sucrose, and fructose (in the analyzed literature, respectively 1.2, 0.6 and 0.6 g/min, ratio 2:1:1, for total carbohydrate intake rate to 2.4 g/min; however, note the higher amounts of ingested carbohydrates).

Maltodextrin and fructose

High oxidation rates are also observed with combinations of maltodextrin and fructose, in the same conditions of the ingestion of glucose plus fructose (therefore, respectively 1.2 and 0.6 g/min, ratio 2:1, for total carbohydrate intake rate to 1.8 g/min).

Such high oxidation rates can be achieved with carbohydrates ingested in a beverage, in a gel or in a low-fat, low protein, low-fiber energy bar.

The best combination of carbohydrates ingested during exercise seems to be the mixture of maltodextrin and fructose in a 2:1 ratio, in a 5% solution, and in a dose around 80-90 g/h.

Maltodextrin and Fructose: Oxidation of Ingested Carbohydrates
Fig. 1 – Oxidation of Ingested Carbohydrates

Why?

  • This mixture has the best ratio between amount of ingested carbohydrates and their oxidation rate and it means that smaller amounts of carbohydrates remain in the stomach or gut reducing the risk of gastrointestinal complication/discomfort during prolonged exercise (see brackets grafa in the figure).
  • A solution containing a combination of multiple transportable carbohydrates and a carbohydrate content not exceeding 5% optimizes gastric emptying rate and improves fluid delivery.

Example of a 5% carbohydrate solution containing around 80-90 g of maltodextrin and fructose in a 2:1 rate; ingestion time around 1 h.

  • 1.5 L solution: 80 g of carbohydrates, including around 55 g of maltodextrin and around 25 of fructose.
  • 1.8 L solution: 90 g of carbohydrates, including 60 g of maltodextrin and 30 of fructose.

Conclusion

During prolonged exercise, when high exogenous carbohydrate oxidation rates are needed, the ingestion of multiple transportable carbohydrates is preferred above that of large amounts of a single carbohydrate.
The best mixture seems to be maltodextrin and , in a 2:1 ratio, in a 5% concentration solution, and at ingestion rate of around 80-90 g/h.

References

Burke L.M., Hawley J.A., Wong S.H.S., & Jeukendrup A. Carbohydrates for training and competition. J Sport Sci 2011;29:Sup1,S17-S27. doi:10.1080/02640414.2011.585473

Jentjens R.L.P.G., Moseley L., Waring R.H., Harding L.K., and Jeukendrup A.E. Oxidation of combined ingestion of glucose and fructose during exercise. J Appl Physiol 2004:96;1277-1284. doi:10.1152/japplphysiol.00974.2003

Jentjens R.L.P.G., Venables M.C., and Jeukendrup A.E. Oxidation of exogenous glucose, sucrose, and maltose during prolonged cycling exercise. J Appl Physiol 2004:96;1285-1291. doi:10.1152/japplphysiol.01023.2003

Jeukendrup A.E. Carbohydrate feeding during exercise. Eur J Sport Sci 2008:2;77-86. doi:10.1080/17461390801918971

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

Prolonged exercise and carbohydrates

During prolonged exercise (>90 min), like marathon, Ironman, cross-country skiing, road cycling or open water swimming, the effects of supplementary carbohydrates on performance are mainly metabolic rather than central and include:

  • the provision of an additional muscle fuel source when glycogen stores become depleted;
  • muscle glycogen sparing;
  • the prevention of low blood glucose concentrations.

How many carbohydrates should an athlete take?

The optimal amount of ingested carbohydrate is that which results in the maximal rate of exogenous carbohydrate oxidation without causing gastrointestinal discomfort”. (Jeukendrup A.E., 2008, see References).

Prolonged exercise: which carbohydrates should an athlete take?

Until 2004 it was believed that carbohydrates ingested during exercise (also prolonged exercise) could be oxidized at a rate no higher than 1 g/min, that is, 60 g/h, independent of the type of carbohydrate.
Exogenous carbohydrate oxidation is limited by their intestinal absorption and the ingestion of more than around 60 g/min of a single type of carbohydrate will not increase carbohydrate oxidation rate but it is likely to be associated with gastrointestinal discomfort (see later).
Why?
At intestinal level, the passage of glucose (and galactose) is mediated by a sodium dependent transporter called SGLT1. This transporter becomes saturated at a carbohydrate intake about 60 g/h and this (and/or glucose disposal by the liver that regulates its transport into the bloodstream) limits the oxidation rate to 1g/min or 60 g/h. For this reason, also when glucose is ingested at very high rate (>60 g/h), exogenous carbohydrate oxidation rates higher 1.0-1.1 g/min are not observed.

Role of nutrition in prolonged exercise

The rate of oxidation of ingested maltose, sucrose, maltodextrins and glucose polymer is fairly similar to that of ingested glucose.

Fructose uses a different sodium independent transporter called GLUT5. Compared with glucose, fructose has, like galactose, a lower oxidation rate, probably due to its lower rate of intestinal absorption and the need to be converted into glucose in the liver, again like galactose, before it can be oxidized.
However, if the athlete ingests different types of carbohydrates, which use different intestinal transporters, exogenous carbohydrate oxidation rate can increase significantly.
It seems that the best mixture is maltodextrins and fructose.

Note: the high rates of carbohydrate ingestion may be associated with delayed gastric emptying and fluid absorption; this can be minimized by ingesting combinations of multiple transportable carbohydrates that enhance fluid delivery compared with a single carbohydrate. This also causes relatively little gastrointestinal distress.

Conclusion

The ingestion of different types of carbohydrates that use different intestinal transporters can:

  • increase total carbohydrate absorption;
  • increase exogenous carbohydrate oxidation;
  • improve performance.

References

Burke L.M., Hawley J.A., Wong S.H.S., & Jeukendrup A. Carbohydrates for training and competition. J Sport Sci 2011;29:Sup1,S17-S27. doi:10.1080/02640414.2011.585473

Jentjens R.L.P.G., Moseley L., Waring R.H., Harding L.K., and Jeukendrup A.E. Oxidation of combined ingestion of glucose and fructose during exercise. J Appl Physiol 2004:96;1277-1284. doi:10.1152/japplphysiol.00974.2003

Jentjens R.L.P.G., Venables M.C., and Jeukendrup A.E. Oxidation of exogenous glucose, sucrose, and maltose during prolonged cycling exercise. J Appl Physiol 2004:96;1285-1291. doi:10.1152/japplphysiol.01023.2003

Jeukendrup A.E. Carbohydrate feeding during exercise. Eur J Sport Sci 2008:2;77-86. doi:10.1080/17461390801918971

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

Carbohydrate ingestion during short duration high intensity exercise

High Intensity: During-Exercise Nutrition
Fig. 1- During-Exercise Nutrition

Carbohydrate ingestion during intermittent high intensity or prolonged (>90 min) sub-maximal exercise can:

  • increase exercise capacity;
  • improve exercise performance;
  • postpone fatigue.

The intake of very small amounts of carbohydrates or carbohydrate mouth rinsing (for example with a 6% maltodextrin solution) may improve exercise performance by 2-3% when the exercise is of relatively short duration (<1 h) and high intensity (>75% VO2max), that is, an exercise not limited by the availability of muscle glycogen stores, given adequate diet.
The underlying mechanisms for the ergogenic effect of carbohydrates during this type of activity are not metabolic but may reside in the central nervous system: it seems that carbohydrates are detected in the oral cavity by unidentified receptors, promoting an enhanced sense of well-being and improving pacing.
These effects are independent of taste or sweet and non-sweet of carbohydrates but are specific to carbohydrates.

It should be noted that performance effects with drink ingestion are similar to the mouth rinse; therefore athletes, when they don’t complain of gastrointestinal distress when ingesting too much fluid, may have an advantage taking the drink (in endurance sports, dehydration and carbohydrate depletion are the most likely contributors to fatigue).

Conclusion
It seems that during exercise of relatively short duration (<1 h) and high intensity (>75% VO2max) it is not necessary to ingest large amounts of carbohydrates: a carbohydrate mouth rinsing or the intake of very small amounts of carbohydrates may be sufficient to obtain a performance benefit.

References

Burke L.M., Hawley J.A., Wong S.H.S., & Jeukendrup A. Carbohydrates for training and competition. J Sport Sci 2011;29:Sup1,S17-S27. doi:10.1080/02640414.2011.585473

Jentjens R.L.P.G., Moseley L., Waring R.H., Harding L.K., and Jeukendrup A.E. Oxidation of combined ingestion of glucose and fructose during exercise. J Appl Physiol 2004:96;1277-1284. doi:10.1152/japplphysiol.00974.2003

Jentjens R.L.P.G., Venables M.C., and Jeukendrup A.E. Oxidation of exogenous glucose, sucrose, and maltose during prolonged cycling exercise. J Appl Physiol 2004:96;1285-1291. doi:10.1152/japplphysiol.01023.2003

Jeukendrup A.E. Carbohydrate feeding during exercise. Eur J Sport Sci 2008:2;77-86. doi:10.1080/17461390801918971

Carotenoids: definition, structure and classification

Carotenoids
Fig. 1 – Carrots

Carotenoids are soluble-fat pigments found throughout nature.
Carotenoids were discovered during the 19th century.
In 1831 Wachen proposed the term “carotene” for a pigment crystallized from carrot roots.
Berzelius called the more polar yellow pigments extracted from autumn leaves “xanthophylls” (originally phylloxanthins), from Greek words xanthos, meaning yellow, and phyllon, meaning leaf.
Tswett separated many pigments and called them “carotenoids.”
They occur in the chromoplasts of plants and some other photosynthetic organisms such as algae and in some types of fungi and bacteria; they are also produced by some invertebrates (Aphids).
There are more than 750 different carotenoids ranging in color from red (such as lycopene), to orange (such as alpha-carotene, beta-carotene, and gamma-carotene) or yellow (such as lutein, alfa-cryptoxanthin or violaxanthin); more than 100 have been found in fruits and vegetables.
In some green plants and in their parts, generally the darker the green color, the higher the carotenoid content: for example, carotenoid content in pale green cabbage is less than 1% of that in dark green one.
Fruit carotenoids are very different, and those present in ripe fruits may be different from those present in unripe fruits.
They also occur extensively in microorganisms and animals.
In plants, microorganism and animals carotenoids have diverse and important functions and actions.

CONTENTS

Chemical structure of carotenoids

Carotenoids are a class of hydrocarbon compounds consisting of 40 carbon atoms (tetraterpenes), with a structure characterized by an extensive conjugated double-bond system that determines the color (it serves as a light-absorbing chromophore): as the number of conjugated double-bond increases, color changes from pale yellow, to orange, to red.
In nature, they exist primarily in the more stable all-trans isomeric configuration, even though small amounts of cis isomers do occur too (they can be produced from all-trans forms also during processing).
Traditionally, carotenoids have been given trivial names derived from the biological source from which they are extracted. However, a semisystematic scheme exists: it allows carotenoids to be named in a way that describes and defines their structure.

Classification

Depending on the presence or absence of oxygen in the molecule, they can be divided into:

  • xanthophylls, which contain oxygen, such as:

Antheraxanthin
Astaxanthin (red)
Auroxanthin
Bixin, E160b
Canthaxanthin (red), E161g
Capsanthin, E160c
Capsorubin, E160c
beta-Carotene-5,6-epoxide
alfa-Cryptoxanthin (yellow)
beta-Cryptoxanthin (orange)
Crocetin
Lutein (yellow), E161b
Lutein-5,6-epoxide or taraxanthin
Luteoxanthin
Lycophyll
Lycoxanthin
Neoxanthin
Rubixanthin
Tunaxanthin
Violaxanthin (yellow)
Zeaxanthin (yellow-orange)
Zeinoxanthin

  • carotenes, which lack oxygen, as such:

alfa-Carotene (orange)
beta-Carotene (orange), E160a
delta-Carotene
gamma-Carotene (orange)
Lycopene (red), E160d
Neurosporene
Phytoene (colorless)
Phytofluene
alfa-Zeacarotene
beta-Zeacarotene
zeta-Carotene

Depending on chemical structure they can be divided into:

  • acyclic carotenes: formed by a linear carbon chain such as:

zeta-Carotene
Phytoene (colorless)
Lycopene (red), E160d
Neurosporene
Phytofluene

  • cyclic carotenes: containing one or two cyclic structures such as:

alfa-Carotene (orange)
beta-Carotene (orange), E160a
gamma-Carotene (orange)
delta-Carotene
alfa-Zeacarotene
beta-Zeacarotene

  • hydroxycarotenoids (or carotenols): containing at least an hydroxyl group (xanthophylls) such as:

alfa-Cryptoxanthin (yellow)
beta-Cryptoxanthin (orange)
Lutein (yellow), E161b
Lycofill
Lycoxanthin
Rubixanthin
Zeaxanthin (yellow-orange)
Zeinoxanthin

  • epoxycarotenoids: containing at least an epoxic group (xanthophylls) such as:

Antheraxanthin
Auroxanthin
beta-Carotene-5,6-epoxide
Lutein-5,6-epoxide
Luteoxanthin
Neoxanthin
Violaxanthin (yellow)

  • uncommon or species-specific carotenoids such as:

Bixin, E160b
Capsanthin, E160c
Capsorubin, E160c
Crocetin

Note: Although green leaves contain unesterified hydroxycarotenoids, most carotenols in ripe fruits are esterified with fatty acids. However, those of some fruits, particularly those that remain green when ripe (example kiwi fruit) undergo no or limited esterification.

Apocarotenoids

Apocarotenoids are a class of carotenoids containing less than 40 carbon atoms, very widespread in nature and with extremely different structures.
They derive from 40 carbon atom carotenoids by oxidative cleavage that can occurs through non-specific mechanisms, such as photo-oxidation, or through the action of specific enzymes (these enzymatic activities, identified in plants, animals and microorganisms, are collectively referred to as carotenoid cleavage dioxygenases).
Some of the most well-known

  • vitamin A
  • abscisic acid
  • bixin, E160b
  • crocetin
  • trans-β-apo-8′-carotenal, E160e

References

Boileau A.C., Merchen N.R., Wasson K., Atkinson C.A. and Erdman Jr J.W. cis-Lycopene is more bioavailable than trans-lycopene in vitro and in vivo in lymph-cannulated ferrets. J Nutr 1999;129:1176-1181. doi:10.1093/jn/129.6.1176

de la Rosa L.A., Alvarez-Parrilla E., Gonzàlez-Aguilar G.A. Fruit and vegetable phytochemicals: chemistry, nutritional value, and stability. 1th Edition. Wiley J. & Sons, Inc., Publication, 2010

Engelmann N.J., Clinton S.K., and Erdman Jr J.W. Nutritional aspects of phytoene and phytofluene,carotenoid precursors to lycopene. Adv Nutr 2011:2;51-61. doi:10.3945/​an.110.000075

Olempska-Beer Z. Lycopene (synthetic): chemical and technical assessment (CTA). Office of Food Additive Safety, Center for Food Safety and Applied Nutrition. U.S. Food and Drug Administration. College Park, Maryland, USA.

Periago M.J., Bravo S., García-Alonso F.J., and Rincón F. Detection of key factors affecting lycopene in vitro accessibility. J Agr Food Chem 2013;61(16):3859-3867. doi:10.1021/jf3052994

Ross A.B., Thuy Vuong L., Ruckle J., Synal H.A., Schulze-König T., Wertz K., Rümbeli R., Liberman R.G., Skipper P.L., Tannenbaum S.R., Bourgeois A., Guy P.A., Enslen M., Nielsen I.L.F., Kochhar S., Richelle M., Fay L.B., and Williamson G. Lycopene bioavailability and metabolism in humans: an accelerator mass spectrometry study. Am J Clin Nutr 2011;93:1263-1273. doi:10.3945/ajcn.110.008375

Wang X-D. Lycopene metabolism and its biological significance. Am J Clin Nutr 2012:96;1214S-1222S. doi:10.3945/​ajcn.111.032359

Hydration before endurance sports

Pre-hydration
Fig. 1 – Pre-hydration

In endurance sports, like Ironman, open water swimming, road cycling, marathon, or cross-country skiing, the most likely contributors to fatigue are dehydration and carbohydrate (especially liver and muscle glycogen) depletion.

Pre-hydration

Due to sweat loss needed to dissipate the heat generated during exercise, dehydration can compromise exercise performance.
It is important to start exercising in a euhydrated state, with normal plasma electrolyte levels, and attempt to maintain this state during any activity.
When an adequate amount of beverages with meals are consumed and a protracted recovery period (8-12 hours) has elapsed since the last exercise, the athlete should be euhydrated.
However, if s/he has not had adequate time or fluids/electrolytes volume to re-establish euhydration, a pre-hydration program may be useful to correct any previously incurred fluid-electrolyte deficit prior to initiating the next exercise.

Pre-hydration program

If during exercise the nutritional target is to reduce sweat loss to less than 2–3% of body weight, prior to exercise the athlete should drink beverages at least 4 hours before the start of the activity, for example, about 5-7 mL/kg body weight.
But if the urine is still dark (highly concentrated) and/or is minimal, s/he should slowly drink more beverages, for example, another 3-5 mL/kg body weight, about 2 hours before the start of activity so that urine output normalizes before starting the event.

It is advisable to consume small amounts of sodium-containing foods or salted snacks and/or beverages with sodium that help to stimulate thirst and retain the consumed fluids.
Moreover, palatability of the ingested beverages is important to promote fluid consumption before, during, and after exercise. Fluid palatability is influenced by several factors, such as:

  • temperature, often between 15 and 21 °C;
  • sodium content;
  • flavoring.

And hyper-hydration?

Hyper-hydration, especially in the heat, could improve thermoregulation and exercise performance, therefore, it might be useful for those who lose body water at high rates, as during exercise in hot conditions or who have difficulty drinking sufficient amounts of fluid during exercise.
However there are several risks:

  • fluids that expand the intra- and extra-cellular spaces (e.g. glycerol solutions plus water) greatly increase the risk of having to void during exercise;
  • hyper-hydration may dilute and lower plasma sodium which increases the risk of dilutional hyponatraemia, if during exercise, fluids are replaced aggressively.

Finally, it must be noted that plasma expanders or hyper-hydrating agents are banned by the World Anti-Doping Agency (WADA).

Conclusion
“Pre-hydrating with beverages, if needed, should be initiated at least several hours before the exercise task to enable fluid absorption and allow urine output to return toward normal levels. Consuming beverages with sodium and/or salted snacks or small meals with beverages can help stimulate thirst and retain needed fluids” (Sawka et al., 2007, see References).

References

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

Sawka M.N., Burke L.M., Eichner E.R., Maughan, R.J., Montain S.J., Stachenfeld N.S. American College of Sports Medicine position stand: exercise and fluid replacement. Med Sci Sport Exercise 2007;39:377-390. doi:10.1249/mss.0b013e31802ca597

Shirreffs S., Sawka M.N. Fluid and electrolyte needs for training, competition and recovery. J Sport Sci 2011;29:sup1, S39-S46. doi:10.1080/02640414.2011.614269

Hypoglycemia and carbohydrate ingestion 60 min before exercise

Hypoglycemia: Fatigue
Fig. 1 – Fatigue

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.

Strategies to limit hypoglycemia in susceptible subjects

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.

Example: a 5-6% carbohydrate solution, often maltodextrin (i.e. 50-60 g maltodextrin in 1000 ml) or maltodextrin plus fructose (e.g. respectively 33 g plus 17 g in 1000 ml).

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.

Conclusion
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;
  • or avoid carbohydrates 90 min before the onset of exercise.

References

Jeukendrup A.E. Carbohydrate feeding during exercise. Eur J Sport Sci 2008:2;77-86. doi:10.1080/17461390801918971

Jeukendrup A.E., C. Killer S.C. The myths surrounding pre-exercise carbohydrate feeding. Ann Nutr Metab 2010;57(suppl 2):18-25. doi:10.1159/000322698

Moseley L., Lancaster G.I, Jeukendrup A.E. Effects of timing of pre-exercise ingestion of carbohydrate on subsequent metabolism and cycling performance. Eur J Appl Physiol 2003;88:453-458. doi:10.1007/s00421-002-0728-8

Carbohydrate loading before competition

Carbohydrate loading is a good strategy to increase fuel stores in muscles before the start of the competition.

What does the muscle “eat” during endurance exercise?

Muscle “eats” carbohydrates, in the form of glycogen, stored in the muscles and liver, carbohydrates ingested during the exercise or just before that, and fat.
During endurance exercise, the most likely contributors to fatigue are dehydration and carbohydrate 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.);
  • three days of high carbohydrate diet, the so-called carbohydrate loading (a nutritional plan very rich in carbohydrates).

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.
Example of nutritional plan for carbohydrate loading and glycogen supercompensation
Carbohydrate Loading: 2500 kcal Diet

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.

References

Burke L.M., Hawley J.A., Wong S.H.S., & Jeukendrup A. Carbohydrates for training and competition. J Sport Sci 2011;29:Sup1,S17-S27. doi:10.1080/02640414.2011.585473

Hargreaves M., Hawley J.A., & Jeukendrup A.E. Pre-exercise carbohydrate and fat ingestion: effects on metabolism and performance. J Sport Sci 2004;22:31-38. doi10.1080/0264041031000140536

Jeukendrup A.E., C. Killer S.C. The myths surrounding pre-exercise carbohydrate feeding. Ann Nutr Metab 2010;57(suppl 2):18-25. doi:10.1159/000322698

Moseley L., Lancaster G.I, Jeukendrup A.E. Effects of timing of pre-exercise ingestion of carbohydrate on subsequent metabolism and cycling performance. Eur J Appl Physiol 2003;88:453-458. doi:10.1007/s00421-002-0728-8