ENERGY DRINK

Abstract: Sports or energy drink, especially designed to substitute body fluid, carbohydrates, lipids, amino acids and mineral ions during periods of heavy endurance exercise, characterized by its balanced composition of glucose, fructose and maltodextrins, a lipid (MCT-oil) consisting of glycerol esterified with either oleic acid, capric acid or caprylic acid or any combination of capric acid, caprylic acid or saturated laurylic acid, L-carnithine, mineral ions and amino acids with an osmolality not exceeding 300 m-osm/l, in a solution which contains suspended particles of polysaccharides, or droplets of non-solubilized oil, possibly with minor amounts of fruit juice concentrates and artificial flavours. The sports drink ensures sustained levels of blood glucose and minimal expenditure of muscle glycogen, thereby reducing the production and accumulation of lactate. The sports drink also minimizes the reduction in glucagon/insulin ratio, providing an optimal stress hormone status facilitating expenditure of energy rich substrates like medium chain and long chain free fatty acids, and glucose directly extracted from the blood perfusing the muscle.

Description: ENERGY DRINK 1. Introduction In general, sports or energy drinks are designed to ensure sufficient supplies of energy and mineral ions to the working muscle, thereby ensuring an optimalization of sugar, fatty acid and ammo acid consumption Furthermore, the energy replenishment should be aiming at the prevention of hypoglycaemia, which impairs the function of the nervous system Hence, m general, these sports drinks contain mono- and polymeric sugars and salts (of which Na- and K-salts are properly balanced) Recently patented and/or marketed sports drinks are designed to also enhance hepatic glucone- ogenesis by making available to the liver substrates like glycerol, or the ammo acids alanme or glutamine Since the muscular tissue during sustained energy expenditure need access to fatty acids, some researchers have attempted to raise the supplies of free fatty acids by adding medium chain triglycerides = MCT (also given to patients with malabsorption and as parenteral energy supplies to critic ally ill, hospitalized patients) . However, no sports or energy drink with a balanced composition aiming at maximal muscular fatty acid catabol- lsm, reduced lactic acid production, reduced muscular protein catabolism and blockade of central nervous fatigue while utilized during endurance exercise, has hitherto been developed. The present sports drink aims at encompassing all of the above mentioned aspects. The invention constitu¬ tes an optimal composition of energy rich compounds especi¬ ally designed to yield rapidly accessible and sustained muscular and cerebral energy supplies and mineral ions comprising cations like Na, K, Mg and Ca, and anions like Cl , phosphate, bicarbonate, and organic acid ions like succmate, fumarate, citrate, as well as mono- and polyme¬ ric carbohydrates, ammo acids, L-carmthme and lipids, wherein the lipids are comprised of glycerol esterified with a long chain mono- or polyunsaturated fatty acid like oleic acid, and/or capric and/or caprylic and/or a C 12 - fatty acid in which the lipid preferably exists as an oil, and where the ammo acids preferably are ammo acids with a branched side-cham like valine, leucme and/or lsoleucine 2. Biochemical and physiological background 2.1. Metabolism in the contracting muscle Depending on the caloric demand, the metabolic rate of a myocyte can be increased some 200 times, compared to the resting level, This occurs m spite of a small number of metabolic pathways within tne cell. In general, these major pathways comprise. 1) complete oxidation of carbohy¬ drates, fat and proteins (i.e. ammo acids) m the muscle; 2) net transformation of carbohydrates to storage fat, and of proteins to carbohydrates (gluconeogenesis) and fat, 3) net production of keto acids (aceto-acetic acid and β- hydroxy butyric acid (only m liver) , and 4) net degrada¬ tion of carbohydrates (glycogenolysis, anaerobic glyco- lysis) . The cell utilizes four important metabolic pathways to catabolize and extract energy from fat and carbohydrates (see figure 1) . These are the glycolysis, the β-oxidation, the citric acid cycle, and the oxidative phosphorylation. Figure 1 shows the major metabolic pathways ensuring energy production in the myocyte. In the figure each small arrow depicts a chemical (enzymatic) reaction. Enzymes, being mandatory to, and applied as measures of metabolic ca- pacity, are the following: PFK = phosphofructokinase, LDH = lactate dehydrogenase, HAD = 3-hydroxyacyl-CoA-de- hydrogenase, CS = citrate synthetase, SDH = succmate dehydrogenase. The large arrows indicate entrance points for amino acids, which serve as substrates in a given metabolic pathway. ATP, which is the energy rich compound utilized by the myocyte, can be synthesized in many ways, depending on pertinent demands for muscle force generation. In table 1, some "activities" and estimated energy demands and energy availability to the contracting muscle are summarized. Table I : Activity Energy demand Availability A) Velocity B) Amount Type Amount ♦a********************************************************* 100 m dash 2.6 0.43 ATP+PCr 0.50 400 m 2.3 1.72 ATP+PCr 0.50 800 m 2.0 3.43 Glycolysis 1.50 1500 m 1.7 6.00 Glucose oxid 85.0 Marathon 1.0 150.0 Fatty acid oxid 4000 Rest 0.0 *******+****************★★*****************★**************★ A) energy rich phosphate; mol/min B) energy rich phosphate; mol/70 kg energy rich phosphate equals the sum of ATP and PCr (creatine phosphate) Glucose oxid = glycolysis and oxidation in the citric acid cycle Fatty acid oxid = β-oxidation and oxidation in the citric acid cycle During a limited engagement, the muscles can thrive on its own storage of ATP and creatine phosphate (which re- synthesises ATP from ADP) without de novo production of ATP. During prolonged muscle activity, the expenditure of substrates is gradually shifted towards glycolysis and fatty acid oxidation, which both yield acetyl-CoA, forcing the citric acid cycle to produce reduced flavine and ade- nine nucleotides driving the oxidative phosphorylation in the presence of oxygen (CU) . If a sudden enhancement of energy production is required, ATP is generated from an¬ aerobic glycolysis with concomitant production of lactic acid, because the 0 2 available is not sufficient to in- crease ATP-synthesis by oxidative phosphorylation alone 2.2 Cellular metabolism and physical endurance The most prominent adaptive changes withm a muscle fibre constantly subjected to endurance exercise comprise: 1) activation of metabolic enzymes, 2) altered sensitivity to hormones, 3) a change in the profile of contractile elements (filaments) and 4) optimalization of membrane- bound transport mechanisms. In this chapter, emphasis will be put on issue 1) . A muscle, which is stimulated chronically by elec¬ trical pulses for 2-3 weeks to perform over a prolonged period of time, demonstrates the following adaptive chang es: a) increased activity of the enzymes SDH, CS, HK and HAD and b) a reduction in the enzymes LDH, PFK, phosphoryl- ase and phosphoglucomutase (see figures 2A and 2B) . The first three enzymes are contained withm the citric acid cycle, and will increase the production of NADH, thus increasing the flow through the constituents of oxidative phosphorylation chain to give more ATP HAD enhances the breakdown of fat through β-oxidation of free fatty acids (FFA) , while PFK, pnosphorylase and pnosphoglucomutase all belong to the glycolytic pathway A reduction of these enzymes indicate that the augmented oxidative capacity in the muscle makes ATP-production vi glycolytic degradation of glucose almost superfluous. Also creatine kinase (CK) is down regulated, which indicates that the apparatus meant to sustain ATP-levels during maximal anaerobic exercise (e.g. 100 m dash) is of lesser importance Figure 2 shows the changes (% of control) in enzyme activ¬ ities induced by chronic electric stimulation of rabbit hind limb muscle (10 Hz, over 24 hours, for 3 days to 10 weeks) . Abbreviations are: SDH = succmate dehydrogenase, CS = citrate syntetase, MDH = malate dehydrogenase, LDH = lactate dehydrogenase, PFK = 6-phospho froctokinase, HK = hexokinase, HAD, = 3-hydroxyl CoA-dehydrogenase. The relationship between glycolytic and oxidative capacity is a function of exercise load, and is illustrated in figure 3. In figure 3 there is shown changes in the enzymatic activity in the hind thigh muscle from a rabbitt after electro-stimulation. The filled-in circles represent citrate synthetase and the open circles represent fructose bisphosphatase as in similarity with figure 2. The glyco¬ lytic and the oxidative capacity is measured with fructose bisphosphatase and citrate synthetase, respectively. Past a certain time of exercise, the total oxidative ca- pacity is diminished towards normal level, and the sub¬ sequent result is a decimated glycolytic capacity. This is one important aspect of overtraining, which will be de¬ scribed exhaustively in chapter 3. In the muscle, there are several types of fibres with different glycolytic and oxidative capacities (type I = slow, oxidative; type IIA = rapid, oxidative; type IIB = rapid, glycolytic) . Consequently, by practising different exercise modes and intensities (i.e. continuous or inter- mittent loads) , it is feasible to enhance both oxidative and glycolytic capacities. The amount of fibre type I is mainly genetically determined, however, endurance exercise may convert type IIB into type IIA. Hence, custom designed training programs might direct the appropriate change in metabolic capacity best suited for the kind of activity in question. Noteworthy is the fact that interval training (intermittent anaerobic adaptation) increases the muscular level of creatine phosphate (PCr) and the activity of the enzyme creatine kinase (CK) , thus minimizing the time by which ATP is resynthesised from ADP. The mechanisms behind this adaptation of metabolizing enzymes are many Some of which entail claimed causative relations to reduced ATP, increased ammonia (NH 4 + ) from AMP degradation, reduced 0 2 tension, enhanced sympathomimetic stimulation of nerve cells, or augmented protein kinase C (PKC) activation through the release of mtracellular Ca 2+ in the contracting muscle. The latter theory may account for the possible hormonal (and thereby pharmacological = doping?) intervention of exercise induced adaptation. In spite of the fact that the muscle might be rendered max- imally oxidative by prolonged exercise, it needs supplies of carbohydrates while working, to ensure the capacity for intermittent high efficiency output ("spurts") The ex¬ penditure of sugar by the myocyte depends on 1) the de¬ livery rate of glucose from the blood (synthesized m the liver, gluconeogenesis) 2) the glucose transport rate and 3) the rate of glycogenolysis Liver glucose is stimulated by a high glucagon/msulm ratio and cortisol Thereby, blood glucose is maintained , even though HK (hexokinase) m the muscle "steals" or extracts glucose from the blood stream. The muscle contrac¬ tion, i.e. the increase of cytosolic Ca , stimulates translocation of the glucose transporter GLUT-4, which yields and increased transport rate of glucose into the myocyte. Furthermore, msulm and physical exercise in the long run enhance the plasma membrane levels of GLUT-4 The catabolism of muscle glycogen depends on the activation of glycogen phosphorylase by phosphorylase kinase. The latter is stimulated by Ca (in the working muscle) , cAMP (a hormone = adrenaline; glucagon - induced second messenger) , and low pH (acidified muscle due to the accumulation of lactic acid) . Nevertheless, PFK (phospho- fructokmase) is regarded the rate limiting factor and coordinator of muscular glucose expenditure (see figure 4) Figure 4 shows the regulation of glycogenolysis and glycolysis m the myocyte. PFK (phosphofructokmase) regu¬ lates the production of triose phosphates and pyruvate (the entrance to the Krebs cycle = citric acid cycle) Nota¬ tions: + = stimulation, - = inhibition. Even if PFK is reduced by prolonged exercise, the enzyme will still be able to deliver substrate (F1,6DP) to the glycolytic pathway when necessary, due to a low cellu¬ lar level of ATP and citrate. Furthermore, PFK can be inhibited by the accumulation of protons m the myocyte (vis lactic acid production) , or be stimulated by NH 4 + - production from ammo acid catabolism m the muscle cell. Finally, it should also be mentioned that cAMP (i.e. glucagon- or adrenaline-stimulation) inhibits PFK. The importance of fatty acid oxidation for prolonged muscular activity is already described in connection with adaptation phenomena, yielding enhanced oxidative enzyme capacity. Nevertheless, mobilization of free fatty acids (FFA) is slow. Physical exercise lowers the re-esterifi- cation of FFA to glycerol in adipose tissue. Furthermore, the level of lipσprotem lipase = LPL and hormone sensitive lipase = HSL governed by stress hormone/insulin ratio d e. the net effect of cAMP) stimulate net hydrolysis of tri- glycerides, and thereby enhance the blood levels of FFA (maximally 2-3 times increase) . In spite of augmented FFA availability, the uptake of FFA is not altered much. By adaptation and an enhanced access of long-chain FFA, the myocyte may maximally retrieve 2/3 of its total energy from β-oxidation. The pre-existence of large glycogen depots and intermittent intake of sugars are therefore important . However, the myocyte has an intrinsic ability to spare glycogen, since β-oxidation yields large levels of acetyl- CoA, which will inhibit pyruvate dehydrogenase and PFK. 2.3 Physiological aspects of endurance exercise Adaptation of the muscle cell to face enhanced working capacity also demands adjustment of other organ systems for optimal energy utilization. Some of these phenomena are outlined underneath. 2.3.1. Short term exercise The cardiovascular system Heart rate (HR) and stroke volume (SV) increase to yield a minute volume (Q = HR x SV) enhancement ranging from 5 1/mm to 40 1/mιn. Furthermore, the arterio-venous oxygen difference (a-v 0 2 ) increases from 5 ml/dl to 15 ml/dl due to enhanced oxygen consumption. The blood stream is diverted towards the working muscles due to sympatho- adrenergically relaxed arteπoles in the muscle tissue, while arterioles in other tissues, e.g. internal organs, are constricted. The blood volume is slightly diminished due to increased transpiration and enhanced hydrostatic pressure, The body temperature is slightly increased, while blood pH is lowered due to the Cory cycle (production of lactate m the muscle and transport to the liver via the circulation) , or to the production of ketone bodies. Conse¬ quently, the release of 0 2 from haemoglobin is facilitated peripherally (The Bohr effect = saturation curve shift) Respiratory response The amount of air (Vg) exchanged by the lungs increase markedly from 5 1/mιn to 140 1/mιn. V E depends on the vital capacity (VC) , and is not a proper index for the monitoring of fitness. Metabolic response The oxygen uptake (V Q2 ) is enhanced fro approximately 3.5 ml/kg/mm to as high as 90 ml/kg/rrαn. 2.3.2 Endurance exercise Adaptation withm the muscle cell There is an increased mobilisation of motoπc units due to a natural resistance in complementary muscle groups This phenomenon confers a higher precision or co-ordination of nervous firing activity, and thereby enhanced muscular force. Hypertrophy of the muscle tissue, i.e. and enhanced levels of actm and myosin (contractile proteins) , and a strengthening of ambient connective tissue will start developing over time. It has also been asserted that hyper- plasia (increased number of muscle cells) will eventually take place subsequent to prolonged physical activity. The cardiovascular system The heart rate (HR) at rest is often chronically low (30-40 beats/mm) , which can be ascribed to a reduction m sympathetic activity of the autonomous nervous system, and/or a lower frequency of the pace-maker signal of the smoidal node. The stroke volume (SV) is chronically ele¬ vated, which is due to a partial hypertrophic of the heart muscle (predominantly the ventricles) or also enhanced Ca 2+ - fluxes and Ca -myosin ATPase activity. The minute volume (Q) is markedly enhanced, however, mainly because of an increase in the stroke volum (SV) Furthermore, there is ample angiogenesis, i.e. an increase m the amount of muscular capillaries can be observed.. The blood pressure (BP; systole as well as diastole) is moderately lowered. Respiratory response The arterio-venous oxygen difference (a-v 0 2 ) is somewhat increased, however, it is assumed to be linked to an in¬ crease in the number of mitochondria in the myocyte . The pulmonary blood flow is enhanced, but only a minor en¬ hancement of gas volume exchanged (Vg) , vital capacity (VC) or tidal volume can be observed. However, the respiration frequency is markedly reduced. The uptake of oxygen (V Q2 ) is dramatically enhanced, however, this phenomenon is mainly due to the increased blood flow through the muscular tissue . 2.4. Immunological aspects of endurance training Subsequent to an acute enhancement in work load or to intermittent physical activity, one may observe the follow¬ ing alterations in the blood related to adaptations m the function of the immune system.: Increase m leukocyte number (all types) Marked raise in the number of neutrophils Increase in the numner of "killer" (NK) cell Substantial increase m monocyte number B-cells are not significantly affected The number of T-cells (only "helper" cells) is moderately reduced When physical activity ceases, the production of mterleukm 1 (IL-1) and mterleukin 6 (IL-6) is augmented. IL-6 is considered to be involved m the development of osteopenia (reduced bone mass) , which can lead to osteoporosis (bone brittleness) via stimulation of the bone resorbmg osteoclasts in the bone matrix. In general, it may be asserted that physical exercise stimulates our immune system against bacteria, as well as virus and cancer (through the increase in NK cells) . Never- theless, prolonged exercise, which borders on overtraining, may result in the opposite. The amount of leukocytes m the blood is reduced, and the immune defence system is weak¬ ened. The levels of lmmunoglobms belonging to type IgA, IgG and IgM are lowered, and the athletes more easily catch generalized virus infections, upper respiratory tract infections, mononucleosis, gastroenteritis and meningitis. 2.5 Endocrine factors and endurance exercise Endurance exercise does affect the endocrine system, both acutely and in a chronic fashion. The immediate responses may be summarized in figure 5 Figure 5 shows a simplified model of the autonomic endo¬ crine system. ACTH = adenocorticotropic hormone, CNS = central nervous system, GH = growth hormone. The glucagon/msulm ratio determines the cellular glucose uptake and gluconeogenesis m tne liver Further¬ more, insulin is capable of enhancing the transport of ammo acids into the cells and counteract lipolysis m adipose tissue. Adrenaline is an insulin antagonist and stimulates specifically lipolysis, thereby mobilising free fatty acids ((FFA) to the circulation. Adrenocorticotropic hormone (ACTH) from the pituitary augments cortisol pro¬ duction and release from the adrenals, thus enhancing the latent hepatic gluconeogenetic potential. Earlier in this chapter, it is discussed how cAMP-generatmg hormones enhance the rate of glycogenolysis, and how msulm ob¬ literates this effect. Growth hormone (GH) is liberated from the pituitary (facilitated by blood ammo acids and blocked by high glucose) and exerts an msulm-like effect, i.e. it stimulates the uptake of ammo acids into cells, augments protein synthesis and cellular growth. GH also displays an anti-msulm like action, i.e. GH enhances both lipolysis and elevates blood sugar. Finally, the hormonal response to loss of body fluids (e.g. sweating) should be mentioned briefly. Renme from the renal juxta glomerular bodies stimulates the activity of the angiotensm system yielding the vasoactive substance angiotensm II (A-II) , which facilitates the synthesis and liberation of aldosterone from the adrenals, thereby in¬ creasing the reuptake of Na + from the urine to the circula- tion, and reducing the volume of secondary urine (diure¬ sis) . Furthermore, antidiuretic hormone (ADH = vasopressm) from the posterior pituitary lobe) will stimulate the water permeability of tubular cells, thus facilitating water fluxes from the lummal space m the nephrons, and dimmish fluid loss from the body. This is one of the mechanisms utilized by the body to maintain blood pressure during heavy exercise m high ambient temperature. Adaptation due to exercise This is mainly observed as the development of a " spor¬ ts" medulla, which indicates an increased release of adren alme from the adrenals via the autonomic nervous system to stimuli like hypoglycaemia, hypoxia, hypercapma or direct¬ ly via the action of glucagon. Besides, the adapted adren¬ als have increased in size, and render the well trained athlete' s insulin-response to glucose and argmine (and other ammo acids) less prominent. Other pituitary hormones, like luteinizmg hormone (LH) and follicle stimulating hormone (FSH) should also be mentioned, since they play a major role in the production of sex steroids (sex hormones) , and thereby affect the onset puberty and body growth in the early years there¬ after. Intensive physical exercise is associated with a minor reduction in blood volume, and a moderately reduced concen- tration of sex steroids may lead to a pseudo-normal condi¬ tion. Long term endurance exercise will inevitably lead to chronically reduced concentrations of LH, FSH and sex steroids. This condition is designated hypothalamic hypogonadism, and may provoke irregular menstruation in women or reduced spermatogenesis in men. If such a conditi¬ on is precipitated in prepubertal athletes, it may delay the onset of the menarche, and will be directly counter- productive for training of certain physical skills. Oblite¬ ration or loss of pituitary production of gonadotropms may be caused by an overproduction of endogenous opoid peptides (EOP) , e.g. endorphms which will increase their pain threshold, but inhibit the egress of hypothalamic releasing factors, i.e. hormones which normally would stimulate the synthesis and release of LH and FSH from the pituitary. 3. Overtraining Overtraining is due to an imbalance between exercise and restitution, and is defined as a non-expected or non- planned reduction in the ability to perform in the absence of an overt organic ailment or disease, and in spite of a normal or increased training effort or exercise level. Acute overtraining, i.e. a period consisting of a few days until a couple of weeks, is deliberately utilized to attain peak performance subsequent to a few days of rest (= super- compensation) . Chronic overtraining, however, entails a condition where complete recovery or restitution is absent, and where the ability to perform has been reduced, even after several days of rest. At present, there is no simple specific or sensitive diagnostic test applicable to reveal overtraining in an early stage. The diagnosis is based on exclusion of other organic disease. The symptoms of over¬ training can be listed as shown in table 2, and consist of so-called sympathetic or parasympathetic symptom groups: Increased early morning heart rate - Slow normalization of heart (especially rest) frequency subsequent to physical exercise Postural (orthostatic) hypotension Increased blood pressure during rest Slow normalization of resting blood pressure subsequent to physical exercise A reduction in haematocrit (HCT) Reduced working capacity (enhanced fatigue) Amenorrhoea (cessation of menstruation) Reduced V Q2 (blood oxygen saturation) Weight loss Increased tendency to contract infections - Sluggish would healing rate Loss of libido (sexual desire) Loss of appetite Sleep disorders Depressive behavioural patterns - Loss of initiative and enthusiasm Increased nocturnal fluid intake Muscle- and joint pain (heaviness of legs) Increased serum creatine kinase activity Table II Some signs and symptoms of overtraining Acute overtraining (which is a rare condition) occurs with sprinters, jumpers and throwers (anaerobic training) , and usually results m weight loss, sleep disorders, acce¬ lerated resting pulse and delays in regaining normal ca¬ pacity (which resembles hypothyroidism) Chronic over¬ training occurs with cyclists and long distance runners (aerobic training) , and entails predominantly bradycardia with rapidly regained normal capacity (resembles adrenal hypofunctiomng) . 3.2. Metabolic and other disturbances following overtraining Some common metabolic changes associated with overtraining are loss of PCr (creatine phosphate) , lactate accumulation in muscle tissue (i.e. proton-induced destruc¬ tion of enzymes withm the different metabolic pathways eventually generating ATP) , loss of muscle glycogen, depletion of blood glucose, and an increased ratio of tryptophan to ammo acids with branched side chains Why is it that the myocyte cannot utilize solely free fatty acids (FFA) for energy production 7 A marathon run¬ ner' s muscle mass can, from F FA, generate only some 50% of the energy required to obtain a decent result (average = 2.15 hours) . FFA are bound to plasma proteins and trans¬ ported into the cells' mitochondria using the carnithme shuttle mechanism. This phenomenon represents an intrinsic upper limit for the extraction of energy from fat Conse¬ quently, the overtraining syndrome is associated with loss of other energy forms like PCr and muscle glycogen, and with a reduction in blood glucose. Hypoglycaemia contributes to what is termeα central fatigue, i.e the central nervous system demands a re- duction of the total body energy expenditure, and strives to overrun the autonomic nervous system. Usually, the muscle will metabolize sugars and fat, if ample amounts of these sources are present. However, the muscular energy expenditure may be covered by ammo acids (up to 20%) , and preferably the ammo acids with branched side chains like leucme, isoleucine and valine. Especially leucine may be metabolized to alanme, glutamine and aspartic acid to become substrates for gluconeogenesis in the liver, but may also be directly converted, by transammation, to acetyl- CoA for further oxidation in the citric acid cycle m the myocyte itself. Nevertheless, NH3 may accumulate m blood, because the liver is not capable of detoxifying the mole¬ cule by funnelling it through the urea (ornithine-citru- llme) cycle. Hence, NH3 may be entering the brain, leading to neurological symptoms like loss of coordination, ataxia and cramps/coma as an inevitable result. However, there are other symptoms also related to the amino acid metabolism, occurring m conjunction with overtraining, . The branched ammo acids, which are utilized during muscular exercise, are transported into the CNS by the same carrier mechanism used by tryptophan An increased CNS contents of tryptophan is therefore a direct conse¬ quence of strenuous physical exercise. Tryptophan is con¬ verted to the neurotransmitter serotonin (5-HT) , which may accumulate in the CNS leading to an increased sensation of fatigue and a craving for sleep. Enhanced contents of NH 3 in the blood may, by itself, lead to an increased uptake of tryptophan into the CNS (see figures 6A and 6B) . Figure 6a shows the relationship between the metabolism of amino acids containing branched side chain and tryptophan in muscle, liver and brain. Figure 6b shows a schematic representation of peripheral and central fatigue. Notice particularly a) loss of glyco- gen, ATP and PCr (creatine phosphate) in muscle and b) accumulation of 5-HT in the CNS. The production of 5-HT in conjunction with over¬ training may explain several central nervous effects like drowsiness, mood oscillations, fatigue and reduced se¬ cretion of hypothalamic releasing factors like GnRH (go- nadotrophin releasing hormone) , which is responsible for the synthesis and release of LH and FSH from the pituitary. 5-HT is also affecting adrenergic nerve transmission in the CNS, and may lead to serious neuroendocrine related over¬ training problems like hypogonadism in adult athletes, or delayed onset of puberty in juvenile athletes. 4. Overtraining in younger athletes. Older children (14-18 years of age) display tendencies towards a biochemical adaptation in the muscle tissue, as well as increased oxygen uptake, which resemble the phe¬ nomena observed with fully grown athletes. For young male athletes, it is mandatory that they exhibit a normal, age- matched level of testosterone, However, it is not possible to utilize testosterone measurements for prepubertal male athletes to prevent or predict overtraining. Consequently, one has to resort to other variables like diurnal variation of cortisol or growth hormone, sleep disturbances, or measurements of heart rate = HR (which is increased) . If marked alterations of these parameters are manifest, overtraining has already precipitated. This is considered to totally unacceptable with young athletes. But, is if feasible to prevent overtraining in these individuals? If the 5-HT concept is applied as a theory for overtraining, the following deliberation is valid These boys display low testosterone levels m the circulation. Hence, they have low muscle mass, which cannot store large amounts of glycogen. Most probably, their capacity of handling NH 3 in the ornithine-citrullme cycle is reduced, and they may mobilize less FFA due to lesser storage fat than an adult. Consequently, they will experience glycogen depletion, low blood sugar, and NH 3 -intoxication much earlier during physical exercise, than an adult. These young boys also exhibit lower circulating levels of ammo acids (AA) in the blood than adults due to their relatively higher amounts of growth hormone released from the pitui¬ tary. It is therefore more important for young athletes to replenish their glucose pools on a regular basis during exercise, and ingest proteins rich in branched ammo acids (preferably as a hydrolysate) just before finishing their training. Only in this manner, it is then feasible to hamper the uptake of 5-HT to the CNS, thereby preventing a subchronic interference with their natural bodily processes leading to puberty. 5. Rationale for the development of improved energy drinks Conventional energy drinks have focussed on impeding the loss of fluid to ensure optimal blood pressure, inhi¬ biting the development of mitochondrial oedema and myocyte destruction, or restoring the blood sugar to prevent the depletion of blood glucose, which otherwise would decimate glucose metabolism in the central nervous system Further¬ more, it has been attempted to add substrates like glycerol to furnish substrates for the hepatic gluconeogenesis. However, to date, it has not been focussed on the coupling between glycogenolysis and β-oxidation of fatty acids m the muscle, i.e no one has tried to enhance the level of acetyl-CoA via β-oxidation of fatty acids to the extent that glycolysis, and hence, glycogenolysis is obli¬ terated or minimized. It is known that the uptake of free fatty acids (FFA) to the mitochondria is proportional to the FFA blood concentrations, and that the transport of FFA into the mitochondria is dependent on the carnithme-shut- tle mechanism. But, this transport mechanism is restricted to long chain fatty acids Fruit and nut oils contain a larger portion of saturated, medium chain fatty acids (C g , C^ Q and C 12 acids) esterified to glycerol (hereafter desig¬ nated MCT = medium chain triglycerides) MCT fatty acids do not esterification to L-carnithme to ensure uptake into the mitochondrial matrix. Custom designed oils with combinations of C g , C 1Q and C 12 acιc *s together with oleimc acid have been used as a lipid supplementation to patients suffering from malabsorption or as parenteral alimentation, and there is ample proof of the beneficial effects of MCT in healthy volunteers and surgical patients Of results obtained, relevant to the active athlete, should be mentioned that the MCT fatty acids are not mcor- porated into adipose tissue, but are directly utilized for energy production by the skeletal muscle. Furthermore, MCT fatty acids will reduce the release of ammo acids (gluta- mine and alanine) from muscle tissue and thereby impede protein degradation in the myocyte. MCT is transported in the portal vein blood and is therefore brought/delivered quickly to the working muscle, provided that the FFA ex- traction rate of the liver is low. The MCT acids decrease the glucose expenditure in slow-twitch muscle fibres, and hamper the oxidation of glucose withm the myocyte. MCT taken together with a meal does not bring about a signifi¬ cant alteration of blood levels of msulm, C-peptide or glucagon. MCT will, subsequent to prolonged mgestion, reduce body weight and fat depots in rats, and as well as serum- and liver levels of cholesterol. Furthermore, it has been shown that MCT contributes to increased stamina of the heart muscle when oxygen supplies are scarce, and that blood pressure is moderately reduced. A modest stimulation of the immune system has also been observed. It is therefore reasonable to believe that an MCT supplement would contribute to a reduction of glycogeno- lytic activity and glucose expenditure m the muscle to such an extent that muscular work, which otherwise would have been partly anaerobic, thereby increasing the produc¬ tion of lactic acid with ensuing muscle fibre αamage, is tilted m the direction of being aerobic. Hence, an MCT supplement would secure high enough levels of acetyl-CoA from the β-oxidation of FFA to spare the muscular glucose pool . Consequently, the muscle might be rendered aerobic for a prolonged period, thereby preserving the glycogen stores for intermittently enhanced efficiency demands and spurts, to give the athlete an advantage when competing. Furthermore, it is reasonable to expect that MCT supplemen¬ tation will reduce the lactate accumulation in muscle to the extent that the phase of restitution following exercise periods may be shortened, thus delaying the onset of ex- haustion leading to overtraining. As an extra guarantee against overtraining, one may add a small amount of ammo acids, preferably ammo acids with branched side chain These would secure a sufficient supply of ammo acids along with the glycerol released upon MCT hydrolysis (to liberate FFA) to support the hepatic gluconeogenesis necessary to preserve a high blood glucose level. Finally, the branched side chain amino acids would also inhibit the uptake of tryptophan into the CNS, with an ensuing blockage of sub¬ strate for 5-HT synthesis, thus preventing the onset of central nervous fatigue and somnolence. In various muscle model systems, it has been shown that the uptake of fatty acids corresponds to an expendi¬ ture of FFA approximating 12 g/hour per 75 kg body mass, provided a rise in the blood FFA levels to 2-3 mmol/1. Adding a supplement of 4 g of MCT every 20 minute equals a theoretical concentration of 2-3 mmol/1 of C g and C-J_ Q fatty acids alone. The half life of MCT-fatty acid clear¬ ance from the circulation of a person at rest is 17 minut¬ es. This indicates that close to all the ingested MCT (4 g) would be metabolized in 17 x 5 = 85 minutes. In the exer- cising muscle, the metabolic rate may be enhanced up to ten fold, hence 4 g of MCT would normally be taken up and metabolized in far less that 20 minutes. Then, an athlete would utilize all the MCT-fatty acids ingested, provided that the ensuing msulm increase due to concomitant intake of glucose and glucose polymers is not inhibiting the lipoprotem lipase situated in capillary walls withm the muscle tissue. However, it is known that a high level of FFA may lead to ketogenesis in the liver with ensuing acidification of the blood. Concomitant mgestion of glucose has, however, convincingly reduced or fully obliterated the production of ketone bodies in the liver. With the conjunctive intake of fructose, which mainly contributes to the synthesis of citrate and malonyl-CoA in the liver, it is reasonable to anticipate that the hepatic β-oxidation of MCT-fatty acid reaching the hepatocyte will be dramatically reduced, due to the inhibition of hepatic carnithme acyl transferase I (CAT- I) by malonyl-CoA. As a consequence, the ketogenesis would be almost eliminated. 6. Test procedure Eight healthy male volunteers aged 24 to 45 years cycled on an ergometer cycle for 160 consecutive minutes using a pulse metre. The pulse rate was kept at a constant level equalling 80% of maximal attainable pulse rate for each individual. Warm up was conducted for 10 minutes with a maximally permitted pulse rate of 120 beats/mm, and venous blood was drawn using the Venoject system Immedi¬ ately thereafter, 330 ml energy drmk were mgesteα. Every 20 minutes, the procedure was repeated by the test person without him stopping the pedalling during blood sampling and fluid replenishment. The blood sample (plasma) was analysed at the Institute of Medical Biochemistry, Univer¬ sity of Oslo, Norway, for glucose, lactate and β-hydroxy butyric acid, using standard kits obtained from Sigma Chemical Company (USA) . Standard clinical chemistry parame¬ ters and msulm and glucagon were analysed by Furst' s Medical Laboratory (Oslo, Norway) and the Hormone Labora¬ tory, Aker Hospital (Oslo, Norway) . Finally, free fatty acids (FFA) were analysed using standard HPLC technique at the Institute for Chemistry, University of Bergen, Norway. The investigation period was dived into two time units, i.e. the first ordinary cycling exercise was con- ducted using energy drmk without the MCT supplement. After some 14 days, identical experiments were performed, how¬ ever, this time, the energy drmk was fortified with MCT- oils and L-carnithme after 80 minutes of cycling. The objective was to assess how an MCT supplement of 12 grams of Oleum Neutrale = Triglyceπda saturata media (obtained from Norsk Medicinal Depot, Oslo, Norway) containing medium chain fatty acids (C g and C 1Q ) might affect blood glucose and lactate levels after a period of strenuous physical exercise bordering on the anaerobic threshold. 7. Results Example 1 Energy drink for common use: Substance: g/1 ready to drink Glucose 10 Fructose 10 Dextrin 10 15 Dextrin 20 15 Pectin (E440) 0.5 NaCl 0.5 KH 2 P0 4 0.5 K 2 HP0 4 0.5 Valine 1 Leucine 1 L-carnithine 1 Oleum Neutrale 12 Na-carboxy-methyl cellulose (E466) Blood glucose levels remained approximately constant from the 80th to the 160th minute subsequent to intake of the energy drink supplemented with MCT-oil, and at the end of 160 minutes of bicycling, the net gain in blood glucose was some 1.5 mmol/1 (see result-figures 1 and 3) . Lactate accumulation in the blood was dramatically reduced due to intake of energy drink with MCT-oil, and maximal net reduction accomplished at the end of 160 min¬ utes of bicycling was some 15 mmol/1 (see result-figures 2 and 3) . This indicates that the lactate production in the muscle tissue is hampered, i.e. the expenditure of muscle glycogen is diminished. The intake of fluid and salt ions is directed towards maintaining blood volume and replenish electrolytes. Anal¬ yses of , Na, K, Cl and Ca (of which the latter is paralle¬ lled by Mg) before and after each 80 minutes interval, un- disputably showed that the concentrations of each electro¬ lyte did not change during exercise maintained at 80% of maximal aerobic capacity (see result-tables 1 and 2) . Furthermore, the MCT-oil supplement did not at all alter blood electrolytes . The evaluation of short term effects of the energy drink with and without the addition of MCT-oil comprised analyses of haemoglobin (Hb) , erythrocyte sedimentation rate (SR) , liver function tests (blood ALAT, ASAT and albumin) , kidney function tests (blood urea, creatinine, albumin) , cholesterol metabolism (total- and HDL-choleste- rol) , as well as an assessment of myocyte destruction (blood creatine kinase = CK activity) . Irrespective of supplementation of the energy drink with MCT-oil or place- bo, all but one tolerance parameters mentioned were main¬ tained within normal ranges and essentially unaltered, (see result-tables 1 and 2) . Plasma CK, however, increased somewhat during the exercise period, but did not exceed levels normally encountered after periods with strenuous muscular endurance activity. Increased amounts of amino acids in the blood stream after hard endurance exercise is a clear indication of degraded muscle protein, which is unfavourable during a phase when the athlete is building power and form. However, increased intake of amino acids will, when the amino acids are not utilized for the purpose of de novo protein syn¬ thesis, enhance the biochemical load on the liver by for¬ cing it to increase its synthesis of urea. Monitoring of urea after each 80 minute period demonstrated that each test individual did not produce or retain more urea sub¬ sequent to the intake of energy drink with supplementation of ammo acids, as compared with zero time analyses (see result-tables 1 and 2) . If the levels of msulm enhance rapidly as a result of enhanced intake of sugars, ammo acids or fat (like after a well balanced meal) , gluconeogenesis is impeded, and the mobilization of fat from adipose tissue and the hydrolysis of triglyceπdes in lipoprotem particles are hampered. Hence, we investigated whether or not plasma insulin and glucagon levels were significantly altered every 20 minutes during the total period of bicycling (160 minutes) Result-figures 4 and 5 demonstrate that supple¬ mentation of MCT-oil does not affect the hormone levels in the circulation, and that the msulm level does not m- crease by more than 20% during the first 60-80 minutes after intake of energy drmk with MCT-oil. This indicates that the hepatic gluconeogenesis with amino acids, lactate and glycerol as substrates is intact and well functioning. At the same time, the lipoprotem lipase in the capillaries perfusing the muscles, is also functioning properly, en¬ suring that the MCT-oil is hydrolysed into free fatty acids, which can be utilized directly m the myocytes to produce energy for the muscle contraction. By adding L-carnithme. The mitochondrial uptake of endogenous long chain fatty acids will be facilitated via the shuttle mechanism, without hampering the uptake of the MCT acids. Maximal β-oxidation of the FFA is therefore ensured, which yields a maximally attainable level of acetyl-CoA, which via NADH-synthesis in the Krebs cycle will replenish ATP levels through oxidative phosphoryla¬ tion. Concomitantly, the key enzymes of the glycolytic pathway will be maximally inhibited in an allosteric fashi¬ on by negative feedback from NADH, ATP, acetyl-CoA, ci- trate, and AMP. In this manner, the muscle will save glyco¬ gen until needed for sudden and intermittent increases in energy demands (above the aerobic level) , thereby pre- venting the acidification of the internal myocyte environ¬ ment by lactic acid production. Consequently, one might postulate that the development of muscle stiffness is delayed, and the phase of muscle restitution between exer- cise periods and/or competitions may be shortened. Intake or mobilisation of triglycerides may result m higher levels of FFA m the blood, which may initiate ketogenesis m the liver, thereby reducing blood pH analo- gous to the accumulation of lactic acid m the muscle tissue Consequently, the levels of β-hydroxy butyric acid in the circulation were investigated (see result-figure 6) The analyses demonstrate that mgestion of energy drmk with MCT-oil during bicycling, m fact, reduces blood levels of ketone bodies to approximately zero value. The two fatty acids m Oleum Neutrale exhibit inter¬ mediary chain length, and it is asserted that such fatty acids are not stored by the adipose tissue, but mainly catabolized by the muscle tissue. The levels of tri¬ glycerides and saturated Co and C-, Q fatty acids during bicycling after mgestion of energy drmk supplemented with MCT-oil were estimated (see result-figure 7) . The analyses clearly showed that the plasma levels of triglycerides were not significantly altered, while the concentration of both intermediary chain length fatty acids were reduced to trace amounts (less that 0.1%) withm 20 minutes subsequent to intake of fluid. Since the energy drmk with MCT supplement renders the body favourable m terms of glucagon/msulm ratio, it is concluded that the saturated Cg and C-, Q acids are combusted by the muscle tissue during this 20 minute period L-carnithine esterified to long chain fatty acids facilitates the fatty acid transport into the mitochondria where β-oxidation takes place. The effect of L-carnithme fortification was analysed as a reduction of FFA in plasma (i.e. the reduction in the amount of C 14 , C lg , C lg and C 20 fatty acids with <,2 double bonds) Result-figure 8 clearly shows that the addition of MCT-oil and L-carnithme at the 80th minute reduce the plasma levels of FFA by some 20% starting at the 100th minute of the bicylce exercise. Examples 2-16 Energy drmk, as m example 1, where either glucose, fructose, the dextrms, the ammo acids or the L-carni- thme, either separately or m 2 by 2 combinations, are reduced by 50%, but still contains 12 g/litre of Oleum Neutrale. Other components (i.e salts/electrolytes and additives) are unchanged. The investigation was repeated, as described in ex¬ ample 1, with the same healthy male volunteers bicycling for 160 minutes, using the same work load, fluid mgestion, and venous blood sample delivery every 20 minutes. Blood samples were only analysed for glucose and lactate. The benefits in blood glucose stabilization and circu¬ lating lactate suppression were diminished by some 15-40% and 15-35%, respectively The lowest effect reduction was obtained after removing half the level of ammo acids, the highest effect reduction by removing half the amount of maltodextrm 10 (results not shown) . Example 17 Energy drmk where the MCT-oil was reduced to 8 g/li- tre. Otherwise, the ingredients were as in example 1. The investigation was repeated, as described in ex¬ ample 1, with the same healthy male volunteers bicycling for 160 minutes, using the same work load, fluid mgestion, and venous blood sample delivery every 20 minutes. Blood samples were only analysed for glucose and lactate. The benefits m blood glucose stabilization and circu¬ lating lactate suppression were diminished by some 50% and 45%, respectively (results not shown) . Example 18 Energy drmk where the MCT-oil was enhanced to 15 g/litre. Otherwise, the ingredients were as m example 1. The investigation was repeated, as described in ex¬ ample 1, with the same healthy male volunteers bicycling for 160 minutes, using the same work load, fluid mgestion, and venous blood sample delivery every 20 minutes. Blood samples were only analysed for glucose and lactate The benefits m blood glucose stabilization and circu¬ lating lactate suppression were not increased by more than approximately 10% (results not shown) . Legends to result-tables and result-figures (example 1) Result - table 1 Clinical chemical variables analysed m blood immediately before, 80 minutes after and 160 minutes after mgestion of 330 ml energy drmk every 20 minutes. Energy drink consumed after the 80th minute was supplemented with 12 g/litre of MCT-oil (Oleum Neutrale) The figures obtained for each parameter are given as means ± lxSD for the study popu¬ lation (n = 8) Result - table 2. Clinical chemical variables analysed m blood immediately before, 80 minutes after and 160 minutes after mgestion of 330 ml energy drmk every 20 minutes. No MCT-oil (Oleum Neutrale) was added during the entire study period. The figures obtained for each parameter are given as means ± lxSD for the study population (n = 8) . Result - figure 7 Blood glucose levels during 160 minutes of bicycling The broken line represents mgestion of fluid without addition of MCT-oil. The unbroken line represents a parallel trial with energy drmk fortified with 12 g/litre of MCT-oil subsequent to the 80th minute The figures obtained are given as means ± lxSD for the study population (n = 8) . Result - figure 8 Blood lactate levels during 160 minutes of bicycling. The broken line represents mgestion of fluid without addition of MCT-oil. The unbroken line represents a parallel trial with energy drmk fortified with 12 g/litre of MCT-oil subsequent to the 80th minute The figures obtained are given as means ± lxSD for the study population (n = 8) . Result - figure 9. Differences m blood glucose and lactate levels as a func¬ tion of supplementation of the energy drink with 12 g/litre MCT-oil (as depicted in result-figures 1 and 2) after 80 minutes of bicycling. The unbroken line illustrates the blood glucose difference, while the broken line depicts the lactate difference. Result - figure 10 Blood msulm levels during 160 minutes of bicycling, where the unbroken line represents intake of energy drink without the addition of MCT-oil. The broken line depicts a parallel trial with MCT-oil supplementation of 12 g/litre after the 80th minute. The figures obtained are given as means + lxSD for the study population (n = 8) Result - figure 11. Blood glucagon levels during 160 minutes of bicycling where the unbroken line represents intake of energy drmk without the addition of MCT-oil. The broken line depicts a parallel trial with MCT-oil supplementation of 12 g/litre after the 80th mmute. The figures obtained are given as means ± lxSD for the study population (n = 8) . Result - figure 12. Blood β-hydroxy butyric acid levels during 160 minutes of bicycling where the unbroken line represents intake of energy drmk wit the addition of 12 g/litre MCT-oil after the 80th mmute The figures obtained are given as means ± lxSD for the study population (n = 8) Result - figure 13 Blood tπglyceride levels during 160 minutes of bicycling where the broken line represents intake of energy drmk without the addition of MCT-oil and L-carnithme . The unbroken line depicts a parallel trial with MCT-oil supple¬ mentation of 12 g/litre and an addition of L-carnithme of 1 g/litre after the 80th mmute. The figures obtained are given as means ± lxSD for the study population (n = 8) . Result - figure 14 Blood free fatty acid levels (estimated as the sum of C 14 , C 16' C 18 an( ^ C 20 f att y a cι ds with ≤2 double bonds ) during 160 minutes of bicycling where the broken line represents intake of energy drmk without the addition of MCT-oil and L-carnithme . The unbroken line depicts a parallel trial with MCT-oil supplementation of 12 g/litre and an addition of L-carnithme of 1 g/litre after the 80th minute. The figures obtained are given as means ± lxSD for the study population (n = 8) . Table 1 . Clinical chemistry during exercise with the addition of lipid Table 2. Clinical chemistry during exercise without the addition of lipid References concerning the biochemical/physiological back¬ ground and documentation of MCT in a medical context Biochemistry/Physiology Books : Scientific basis for athletic conditioning (eds. Fisher and Jensen) , Lea & Febiger, Philadelphia, 1990 Endurance m sport (eds. Shophar and Astrand) , Blackwell Scientific Publications, Oxford, 1992 Tidsskriftet for den Norske Lageforenmg : 6 , 1993 ; 113 : 719-22, Bahr et al . , Overtrenmg blant ldretts- utøvere - arsaker, diagnostikk og behandlmg 7 , 1993 ; 113 : 850-2 , Halvorsen og Endsjø, Infeksjonssykdommer og fysiεk aktivitet Review articles: Bale, The functional performance of children m relation to growth, maturation and exercise, Sports Medicine, 13(3) :- 151- 59, 1992 Banister and Cameron, Exercise-induced hyperammonemia : peripheral and central effects, Int J Sports Med, 11:- 129-42, 1990 Cannon, Exercise and resistance to infection, J Am Physiol Soc, 74 (3) :973-81, 1993 Deschenes et al . , Exercise-induced hormonal changes and their effects upon skeletal muscle tissue, Sports Medicine, 12 (2) : 80-93 , 1991 Elias and Wilson, Exercise and gonadal function, Human reproduction, 8 (10) :1747-61, 1993 Guezennec, Role of lipids on endurance capacity m man, Int J Sports Medicine, 13:114-8, 1992 Hood and Terjung, Ammo acid metabolism during exercise and following endurance training, Sports Medicine, 9(1) - :23-35, 1990 Hultman and Greenhaff, Skeletal muscle energy metabolism and fatigue during intense exercise m man, Sci Progress Edinburgh, 75:361-70, 1991 Lehmann and Keul, Overtraining in endurance athletes: a brief review, Med Sci Sports Exercise, 25 (7) : 854-62 , 1993 Pedersen, Influence of physical activity on the cellular immune system: mechanism of action, Int J Sports Med, 12 :23-9, 1991 Saltm and Astrand, Free fatty acids and exercise, Am J Clin Nutr, 57 (suppl .) : 752-8 , 1993 Stanley and Connett, Regulation of muscle carbohydrate metabolism during exercise, The FASEB Journal, 5:2156- 60, 1991 Documentation of MCT Kolb Sc Sailer, 1984. JPEN J Parenter Enteral Nutr, 8:285- 289 Kelly et al . , 1993. J Clin Invest, 92:91-98 Vukovich et al . , 1993. J Appl Physiol, 75:1513-1518 Nolte et al . , 1994 Acta Physiol Scand, 151:51-59 Turcotte et al . , 1992. Am J Physiol, 262:E791-799 Graham et al., 1991 Am J Physiol, 261:E168-176 Senaris et al. , 1992. Neurosci Lett, 135:80-82 Miles et al . , 1991. JPEN J Parenter Enteral Nutr, 15:37-41 Hwang et al . , 1992. J Nutr Sci Vitammol, 38:127-139 Van Kempen & Odle, 1993. J Nutr, 123:1531-1537 Miura et al . , 1993. Immunology, 78:142-146 Stouthard et al . , 1994. JPEN J Parenter Enteral Nutr, 18:436-431 Brousolle et al . , 1992. Metabolism, 41:1276-1283 Sato et al., 1992. JPEN J Parenter Enteral Nutr, 16:451-454 Eckel et al . , 1992. Diabetes, 41:641-647 Rossle et al . , 1991. Infusionstherapie, 18:167-171 Metges & Wolfram, 1991. J Nutr, 121:31-36 Gogos et al., 1990. Am J Clin Nutr, 51:119-122 Rossle et al . , 1990. Am J Physiol, 258:E944-947 Kaunitz, 1986. J Environ Pathol Toxicol Oncol, 6:115-121 Beaufrere, 1985. Am J Physiol, 149:E175-182 Garfmkel et al . , 1992. J Surg Res, 52:328-333 De Gaetano et al . , 1994. JPEN J Parenter Enteral Nutr, 18:134-140 Ball, 1991. Am J Clin Nutr, 53:916-922 Mascioli et al . , JPEN J Parenter Enteral Nutr, 15:27-31 Puchstem et al . , 1990. Anasth Intensivther Notf Med, 25:87-92 Wolfram et al . , 1989. Z Ernahrungswiss, 28:173-180 Satabin et al . , 1989. Eur J Appl Physiol, 58:583-590 Maclver et al. , 1990. J Hum Hypertomas, 4:485-490 Guezennec, 1992. Int J Sports Med, 13.-Suppl 1;S114-118 Hagermann, 1992. Med Sci Sports Exerc, 24 :Suppl ; S309-314 Coyle, 1992. J Nutr, 122 :Suppl ; 788-795 Stanley & Connett, 1991. FASEB J, 5:2155-2159 Coyle, 1991. J Sports Sci, 9;Spec No;29-52

Claims: Claims 1. An energy supplement, with composition suitable for rapid and prolonged muscular and cerebral energy metabolism comprising physiologically absorbable electrolytes like Na, Mg, Ca, K salts of mono- and divalent anions, preferably Cl, phosphate or anions of physiologically absorbable and non-toxic organic acids like malic acid, succinic acid, fumanc acid and citric acid, as well as, carbohydrates, ammo acids and lipids, wherein the lipid comprises glycer¬ ol esterified with a long chain mono- or polyunsaturated fatty acid (like oleinic acid) and/or caprylic and/or capric acid and or/ a C 12 fatty acid, where the lipid preferably is present in the form of an oil, and that the ammo acids preferably comprise ammo acids with branched side chains, like valine, leucine and/or isoleucme, in¬ cluding ammo acids essential to man 2. Composition, accordmg to claim 1, wherein the carbo- hydrates comprise at least three types of sugars chosen from glucose, fructose and maltodextrms, where the malto¬ dextrms preferably represent maltodextπn types 10 & 20. i Composition, according to claim 2, m which the carbo- hydrates are glucose, fructose and maltodextrms 10 & 20 in the ratio of 1:1:1.5:1.5. 4 Composition, according to claim 2, wherein the carbo¬ hydrates are sucrose and maltodextrms 10 & 20 m the ratio of 2.1.5:1.5 5. Composition, accordmg to all preceding claims, to which L-carnithme is added, either as free base or salt, or as fatty acid-acyl carnithine. 6. Composition, accordmg to all preceding claims, in which the lipid and water comprise a homogenous sol- ution/mixture/suspension. 7. Composition, according to claim 6, wherein the osmotic potential of the mixture does not exceed 300 mosm/litre. 8. Composition, accordmg to claims 6 and 7, m which the concentrations of the various components do not exceed: Carbohydrates - 75 g/1 Lipids - 15 g/1 Ammo acids - 3 g/1 Electrolytes - 100 mmol/1 9. Composition, accordmg to all of the preceding claims, in which the mixture also contains preservation additives, juice concentrates and/or artificial flavours.

Inventors: GORDELADZE JAN OXHOLM, GORDELADZE, JAN, OXHOLM
Applicants: GORDELADZE JAN OXHOLM, GORDELADZE, JAN, OXHOLM
Application year: 1997
Main classification: A23L2
IPC codes: A23L1, A23L2