Carnitin 1000 Mineraldrink

Chargement de L-carnitine

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Increased muscle carnitine levels by supplementing L-carnitine with carbohydrates

Previous discussions about the efficacy of L-carnitine regarding increased lipid oxidation basically argued with the difficulty of reaching higher muscle carnitine levels by supplementation of L-carnitine. It was not before two recent studies, which indeed could prove elevated muscle carnitine after oral supplementation (Stephens, J Appl Physiol, 2006; Stephens, J Physiol, 2013). The interest in increased muscle carnitine levels is based on a subsequent enhanced lipid oxidation for energy provision, thereby sparing muscle glycogen and improve endurance performance.
One of these two studies (Stephens, J Appl Physiol, 2006) concluded, that only after 100 (!) days of oral L-carnitine-carbohydrate supplementation (94 g CHO plus 3 g L-carnitine, twice daily!) increased muscle carnitine levels in an efficacy-relevant level similarly to an infusion could be expected. A more recent study (Wall, J Physiol, 2011) reviewed this hypthesis and demonstrated with a daily intake of 2 x 80 g carbohydrates plus 2 g L-carnitine tartrate (CARNIPURE) muscle carnitine levels could be increased by 21%. But it was necessary to follow this intake scheme during 24 weeks, i.e. 168 days! This very study was performed on 14 moderately trained triathletes, training 3-5 times weekly. The increased muscle carnitine levels after 24 weeks of supplementation resulted in a 35% sparing of muscle glycogen after 30 min on a cycle ergometer with 50% VO2max. This corresponds in fact to the halving of total glycogen use during performance, and consequently increased lipid oxidation. Furthermore, following a 30 min time-trial with 80% VO2max directly afterwards 44% lower muscle lactate levels could be measured! Finally, athletes had to perform another 30 min all-out time-trial where performance was improved by 11% compared to prior supplementation and by 35% compared to the control group!
These are very impressive results! But one has to consider that such a long supplementing protocol with a daily intake of 2 x 80 g of carbohydrates provides 1360 kJ (640 kcal), which have to be calculated into the individual daily energy needs in order to prevent a body mass increase. Indeed, body mass increased in the 7 athletes of the control group by 2.4 kg in average, whereas it remained unchanged in the carnitine group. It remained unclear, if carnitine inhibited weight gain in the supplemental group.

Performance enhancement of carnitine confirmed
A recent study (Stephens, J Physiol, 2013) demonstrated with an identical supplementing protocol (80 g CHO plus 2 g L-carnitine tartrate, twice daily) a 20% increase in muscle carnitine levels already after 12 weeks. Also in this study no weight gain occurred – in contrast to the control group taking the same carbohydrates amount without L-carnitine, which gained almost 2 kg of fat mass! It seems indeed, that the previously suspected fat mass gain caused by the (necessary!) high carbohydrates intake does not occur with concomitant carnitine supplementation.
The enhancement of extensive endurance performance thanks to a 20% increase of muscle carnitine levels, respectively its subsequent increase in lipid oxidation, is proven by earlier studies. Out from gene analyses it could also be demonstrated that 73 out of 187 examined genes related to energy metabolism were expressed to a greater extent in the carnitine group or attenuated in the control group, respectively. In summary, such outcome suggests an overall optimized lipid metabolism by L-carnitine.

Acute vascular effect of L-carnitine without loading
There are indeed previous studies, which found a clear effect of L-carnitine also with short-term supplementation. Some studies demonstrated decreased oxidative stress, lactate, cortisol, creatinekinase, and ammonia levels after physical exertion with L-carnitine supplementation (Galloway, FASEB, 2004; O’Connor, Adv Exp Med Biol, 1990; Spiering, J Strenght Cond Res, 2008). The more pronounced such stress factors, the longer recovery time takes. Obviously, such results cannot rely on increased muscle carnitine levels, but must depend on a vascular effect of circulating carnitine. This point of view is also backed up with an expertise undertaken by the Medical Faculty of the University of Geneva, which states that the recovery-enhancing effects of L-carnitine do not depend on increased muscular levels. Instead, circulating carnitine shall have a vascular protective effect against oxidative damage in micro-blood vessels. It was also outlined in this report that a dosage below 1 g is ineffective. Under this viewing angle the supplementation with L-carnitine in higher doses also shortly prior to physical activity seems advantageous.
But with the above mentioned new studies there is now also proof for a glycogen-sparing effect and a direct performance enhancement grace to increased muscular carnitine levels.

Conclusion and recommendations of combinbine L-carnitine and carbohydrates
An increased muscular carnitine level improves not only aerobic performance (glycogen sparing, increased lipid oxidation) but also anaerobic performance in high-intensity sports (decelerated lactate accumulation). Somewhat critical is yet the necessarily long supplementation combined with a high carbohydrate intake. Evidentially, such a supplementation protocol is not suitable for everybody, but has to be considered case-by-case. In some cases acute shortterm L-carnitine intake may be more appropriate and sufficient.
Most studies applied a supplemental protocol of 2-4 g L-carnitine daily. To increase muscular carnitine, a daily intake of 2 x 2 g L-carnitine tartrate, combined with 80 g of high-glycemic carbohydrates each and during at least 12 weeks, seems necessary as discussed above. The lower threshold for the vascular effect of L-carnitine seems to be at 1 g daily, which also constitutes the regulatory upper limit for dietary supplements in Europe.
A convenient intake means are CARNITIN 1000 or the branded, pure L-carnitine tartrate CARNIPURE, which was also used in the study (Wall, J Physiol, 2011). Because maximum blood levels of carnitine are found 2 ½ to 4 h after supplementation it seems likely that insulin peaks should reached within this time period. If the additional 2 x 80 g of high-glycemic carbs are inappropriate for any reason, it is recommended to combine L-carnitine supplementation with a carbohydrate-reach meal, or carbohydrate products used anyway in the context of physical activity (sports drinks, gels, recovery products). Particularly athletes concerned with weight control should consider such advice. In contrast the necessary high-glycemic carbohydrates can be ingested conveniently, in a concentrated drink, by means of a CARBOLOADER.

Increased fat oxidation targeting weight loss
It is deemed important to note that we were discussing increased lipid oxidation hitherto, in order to spare glycogen stores and improve endurance performance. L-carnitine loading combined with carboloading is not a suitable means to reduce body fat stores and body mass, of course! After all a diet is not meant to maximise lipid oxidation in the muscle cell, but to reduce lipid tissues, like visceral and subcutaneous fat stores. Regarding the discussed study results, it has to be stressed that the absence of body mass gain by supplementing L-carnitine plus increased energy intake (160 g of carbohydrates) daily, does not necessarily mean a reduction of body mass when taking L-carnitine but maintaining energy intake. It is not clear yet, if increased muscular carnitine levels cause a higher fat oxidation not just during physical activity, but also under rest.
L-carnitine’s acute, vascular activity regarding lipid oxidation is postulated to be connected with its buffer function inside and outside the cells, not with an enrichment of carnitine in muscle. This is assumed to improve the use of fatty acids as energy source (see box). Some research suggests an inhibition of a drop in muscle carnitine, or maintaining (not increasing!) circulating (vascular) carnitine levels. Nevertheless, fat oxidation has to be activated by physical exercise in a sufficient manner in order to profit from a buffering effect of carnitine supplementation.
In summary, there are plausible reasons for both an acute (vascular) effect and a chronic (muscle carnitine level) intake of L-carnitine – both for endurance athletes as well as for weight reduction! However, for the latter purpose chronic intake is only recommended without additional carboloading. Please find further product recommendations on the SPONSER website under FIGURE & SHAPE.

Mechanism of L-carnitine in lipid and energy metabolism
Fatty acid transport is often considered the main function of L-carnitine. However, according to existing evidence its pH-buffering activity seems more crucial. L-carnitine stabilises extracellular pH by buffering of coenzyme A (CoA) through formation of acetyl-carnitine. This attenuates the accumulation of acetyl-CoA, thereby upholding the activity of an important enzyme (pyruvate dehyrodgenase) for the carnitine-dependent transport of fatty acids into mitochondria (the «burning site» of fatty acids).
On the intracellular level the amount of free CoA is crucial for the oxidation («burning») of fatty acids in the mitochondria. For example, a fatty acid with 18 carbons (C-18) has to be cut into 9 acetyl units (C-2), whereof each needs a free CoA in order to enter the «Krebs-Cycle». Consequently, CoA demand increases dramatically. L-carnitine can temporarily also bind those C-2 units and maintain the energy producing steps, thereby permitting increased lipid oxidation.

Literature
• O’Connor JE et al. (1990): New roles of Carnitine metabolism in ammonia cytotoxicity. Adv Exp Med Biol 272:183-195.
• Galloway SDR et al. (2004): Effect of 2 weeks supplementation with L-Carnitine-L-Tartrate on plasma ammonia response to exercise. Conference proceedings, FASEB.
• Stephens FB et al. (2006): Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol, 102(3):1065-70.
• Spiering BA et al. (2008): Effects of L-carnitine L-tartrate supplementation on muscle oxygenation responses to resistance exercise. J Strenght Cond Res, 22(4):1130-5
• Wall BT et al. (2011): Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. J Physiol, 589(4):963-73
• Stephens FB et al. (2013): Skeletal muscle carnitine loading increases energy expenditure, modulates fuel metabolism gene networks and prevents body fat accumulation in humans. J Physiol, 591(18):4655-66.

Author: Remo Jutzeler
Head R&D SPONSER SPORT FOOD
Ing. Applied Food Sciences UAS
MAS Nutrition & Health ETHZ

Lactoferrine et fer dans le sport

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Lactoferrin and Iron in Sport - Iron Needs and Consequences of Deficiency

Iron deficiency is considered the most common nutrient deficiency globally. Particularly among female athletes it is widespread with 30-50% affected and dependent on several factors. Symptoms of iron deficiency include anaemia, which in contrast also can occur without iron deficiency, tiredness, floppiness, reduced physical performance and immune function. Increased heart rate and lactate levels may result as well. In Europe, approx. 23% of non-pregnant women, and 13-20% of children, 15% of men and roughly 10% of seniors suffer from anaemia (WHO, 2008), with the assumption of a 50% association with iron deficiency. A recent survey in Spain demonstrated an inadequate daily iron intake in 73% and 23% of the general population in women and men, respectively.

Besides magnesium it is iron, which is considered the most important mineral by athletes. Furthermore, because of its well-known function in oxygen transport an as a blood component it seems plausible to think of iron deficiency in case of premature tiredness and performance decline. Iron is also an important component of many enzymes and thereby involved in the regulation of the energy metabolism. Iron losses due to menstruation is a common reason for female athletes to take iron supplements or even infusions. However, infusions of more than 50 ml are considered as a doping method. Furthermore, the weakness of iron supplementation lies in a very low bioavailability, which therefore demands high dosages but, in turn, this causes side effects such as a constipation. Also adverse interactions with other nutrients may occur. Iron transport within our body takes place by the binding of iron to proteins, e.g. transferrin or lacto(trans)ferrin. The latter occurs mainly in milk as its name implies. Roughly two thirds of total body iron is bound in the red blood cells as haemoglobin. Another quarter of iron is stored as ferritin in liver, spleen and bone marrow. These stores are very fluctuating. In dependence of ferritin stores in blood and liver our body hormonally regulates absorption of dietary iron.

The daily iron needs are calculated from the losses and the bioavailability of dietary iron, which on average is 10%, but highly varies between sources and in dependence on the food matrix. Present nutrition recommendations read 10 to 20 mg iron daily in order to compensate for the 1-2 mg estimated losses. Women of childbearing age, pregnant and lactating women should target the upper range. In athletes, microlesions caused by repeated perturbations of long-distance physical exercise, as well as the use of anti-inflammatory drugs such as Ibuprofen or Voltaren, can provoke additional iron losses. However, there is great interindividual variation on iron losses, which discourages to draw general recommendations thereof.

Dietary iron content
The highest iron contents are found in red meat and liver, further in kernels and seeds. However, the absorption rate of iron from foods depends on several factors, incl. the individual iron status. Body iron is found mainly in three chemical forms. Haem-iron is bound in red blood cells to the protein haemoglobin, and in muscles to myoglobin. Haemoglobin transports iron in the blood, myoglobin in muscles. Haem-iron exists only in animal food and is also the iron form with the highest bioavailability of 15 to 35%, whereas free-form iron is much less absorbed (5 to 12%). Free-form iron (Fe) can occur as di- or tri-valent iron (Fe²⁺, bzw. Fe³⁺) and is also called non-haem iron. Both haem- and non-haem iron occur in animal food.

The absorption of non-haem iron, in contrast to haem-iron, is influenced by various substances and nutrients in a food matrix. Interestingly, particular proteins found in animal food promote also the absorption from non-haem iron. Furthermore, also citric and ascorbic acid (vitamin C) enhance non-haem iron bioavailability. In this respect, about 100 ml orange juice demonstrate a similar effect like 30 g of muscle meat, enhancing the iron absorption rate for about a factor 2 or 3! On the opposite, polyphenols from e.g. coffee or wine are disadvantageous in terms of iron absorption. It is deemed important to note that the ingestion of a sour beverage during a meal, or to drip lemon juice on one's vegetables, is more beneficial than skipping one's cup of coffee after lunch. Even alcohol, due to its stimulating effect and stomach acid production, influences iron absorption positively. This makes it unclear, if wine consumption is positive or negative regarding iron absorption. A very clear negative effect on iron bioavailability have complex-forming phytates from cereals. A fact which puts a big question mark to iron enrichment in breakfast cereals. At least also here the simultaneous intake of vitamin C or sour beverages improves absorption.
Iron malabsorption can also be caused by various conditions, such as celiac disease, stomach surgery, gastrointestinal, heart or kidney diseases, as well as the infection with the bacteria Heliobacter pylori. Vegetarians and vegans have an increased risk of deficiency since the best bioavailable haem-iron is lacking in their diet. Even more, the predominantly used soy as a protein source contains the above-mentioned phytates hindering iron absorption. Consequently, it is of great importance for these population group to pay attention on dietary means to improve non-haem iron absorption.

Iron supplementation
Obviously, a combination of the above factors increase the risk of iron deficiency. For example, a vegetarian female athlete being on a diet, or already with a low body mass, and habitual coffee drinker will have a very high risk of iron deficiency. Iron status is usually determined by analysis of ferritin, which mainly indicates iron store levels. Due to a wide range of normal iron store levels, conclusions on iron deficiency are disputable. First of all, it is important to respect a nutritional behaviour in the frame of a suitable diet regarding optimal iron supply and absorption, prior to any supplementation measures.

It is often very unclear who should be supplemented with how much iron, and gastrointestinal problems are common. Regarding athletes, it is deemed important to note, that iron supplementation only enhances physical performance with existing deficiency. Clinical dosages range between 80-120 mg per day, whereas enriching of foods and food supplements is limited to maximally 14 mg per day. The upper tolerable long-term level without risk is set at 45 mg per day! Besides side effects, high dosages cause also an adverse increase of the oxidative potential and hinder the absorption of other minerals. Because on one hand iron deficiency is prevalent – particularly with women and athletes – but on the other hand high dosages may have adverse effects, it is certainly more advantageous first to improve absorption prior to taking iron supplements.

Lactoferrin – an alternative to iron supplements
Lactoferrin offers a solution to the dilemma of a - necessarily high - intake of supplemental iron in order to cure deficiency and the known potential risks. As already mentioned, lactoferrin is a transport protein binding to iron. Lactoferrin is found in high concentration in the milk of mammals. Beside its complexing and transport function it has also an immuno-modulating, anti-inflammatory and antioxidative effect. One molecule of lactoferrin can bind and transport two iron molecules. In the "natural" state lactoferrin from cow's milk is only partly saturated with iron (15-20%) and called holo-lactoferrin. "Emptied" lactoferrin contains less than 5% iron and is called apo-lactoferrin. The latter is the main form in mother's milk.

Lactoferrin from cow's milk was first applied in mother's milk substitutes. Since 2012, lactoferrin is registered as a Novel Food ingredient and authorised for use in various food categories, mainly with respect to its immuno-modulating properties. Not before recently lactoferrin's function in iron metabolism came into focus. The bioavailability of iron from lactoferrin excels even the highest known bioavailability of iron sulphate (Rezk, 2015): 300 pregnant women received either 250 mg lactoferrin, 150 mg iron sulphate or 250 mg iron fumarate during 8 weeks. The lactoferrin group reached a doubled increase of haemoglobin levels (+30%) compared to the other two groups (+15% and +14%). At the same time lactoferrin resulted in less side effects and better tolerance. Another study on pregnant women with iron deficiency, with and without anaemia, demonstrated that lactoferrin (compared to iron sulphate) improved number of red blood cells, haemoglobin, serum iron and serum ferritin after 30 days (Paesano, 2010). Previously, similar absorption rates of iron and increased haemoglobin, serum ferritin, and serum iron were found with lactoferrin compared to iron sulphate supplementation (Nappi, 2009).

Performance enhancement with lactoferrin
Also in non-pregnant women – precisely in female long-distance runners – lactoferrin could reduce incidences of the usually very common anaemia among this population group. They received either 5 mg iron pyrophosphate with or without 450 mg of lactoferrin during 8 weeks. Also in this study the lactoferrin group showed a higher number of red blood cells, higher serum ferritin and serum iron levels (Koikawa, 2008).

In this very study, also a performance test was included. The athletes had to perform a 3000m run before and after the supplementation period. The starting speed was set at 90% of the average time of all personal best times, increased after 1000m and again after 2000m. Finally, lactic acid accumulation was measured. These values show clearly that the lactoferrin group had a much lesser increase compared to their first run than the iron-only group. In interpretation one can say that the continues evacuation of lactic acid is more efficient after 8 weeks of lactoferrin plus iron supplementation compared to iron solely. One can also conclude that the improved blood and iron values led to less exertion on the 3000m at a given speed, grace to improved oxygen transport and ultimately energy metabolism.

In summary, iron deficiency and concomitant performance decrease, which is common in sports and particularly in women, can be treated more efficient and with fewer side effects by supplemental lactoferrin, also in combination with low-dosed iron and vitamin C. Finally, such a supplementation can also be recommended as a preventive, long-term measure.

SPONSER® offers LACTOFERRIN in easy-to-take capsules. One daily ration of 2 capsules delivers 200 mg of lactoferrin, 14 mg iron (100% NRV) along with 48 mg of vitamin C (60% NRV). Click here to download the full article as a PDF with further studies and graphics.

Literature
• Colombani et al, 2015: Eisen (Fe) & Eisenmangel im Sport, Swiss Forum Sport Nutrition
• Koikawa et al, 2008: Preventive effect of lactoferrin intake on anemia in female long distance runners. Biosci Biotechnol Biochem, 72(4),931-5
• Nappi et al, 2009: Efficacy and tolerability of oral bovine lactoferrin compared to ferrous sulfate in pregnant women with iron deficiency anemia: a prospective controlled randomized study. Acta Obstet Gynecol Scand, 88(9):1031-5
• Paesano et al, 2010: Lactoferrin efficacy versus ferrous sulfate in curing iron deficiency and iron deficiency anemia in pregnant women. Biometals, 23:411-7
• Rezk et al, 2015: Oral lactoferrin versus ferrous sulphate and ferrous fumerate for the treatment of iron deficiency anemia during pregnancy. J Adv Nutr Human Metabol, 2:e740.doi:10.14800/janhm.740
• Samaniego-Vaesken et al, 2017: Iron intake and dietary sources in the Spanish population: Findings from the ANIBES study. Published ahead of print: 10.3390/nu9030203
• Iron depletion in athletes: http://paragraph.com.au/pdf/books/clin-sp-nutr.pdf

Author: Remo Jutzeler
Head R&D SPONSER SPORT FOOD
Ing. Applied Food Sciences UAS
MAS Nutrition & Health ETHZ

Brûler les graisses

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L-Carnitine améliore l'oxydation des graisses et optimise les performances d'endurance

Studien wiesen nach, dass ein erhöhter Muskel-Carnitingehalt eine optimierte Fettoxidation zur Energiebereitstellung und damit einen Glycogen-Spareffekt sowie eine verbesserte Ausdauerleistung bewirkt. Die Folgerung aus einer früheren Studie (1) war, dass mit einer oralen L-Carnitin/Kohlenhydrate-Einnahme (2 x täglich 94 g Kohlenhydrate und 3 g L-Carnitin) erst nach 100 Tagen ein mit einer Infusion vergleichbarer und wirkungsrelevanter Anstieg des Muskel-Carnitingehalts zu erwarten sei. Eine neuere Studie (2) hat dann diese Hypothese überprüft und konnte zeigen, dass mit der Einnahme von 2 x täglich 80 g Kohlenhydraten plus 2 g L-Carnitintartrat (CarniPure) der Muskel-Carnitingehalt um 21% erhöht werden kann. Allerdings waren dafür 24 (!) Wochen Supplementierung nötig.

Beeindruckende Resultate
Diese Studie wurde an 14 mässig trainierten Triathleten durchgeführt, welche 3-5 x pro Woche trainierten. Der nach 24 Wochen Supplementierung erhöhte Muskel-Carnitingehalt führte zu einer Einsparung an Muskelglycogen von 35% nach 30 Minuten auf dem Fahrrad-Ergometer bei einer Belastungsintensität von 50% VO2max. Dies bedeutete eine Halbierung des Glycogenverbrauchs während der Belastung, was gleichzeitig eine entsprechend erhöhte Nutzung der Fettverbrennung bedeutete. Weiter wurde nach der direkt anschliessenden 30-minütigen Belastung bei 80% VO2max ein um 44% tieferer Laktatgehalt in der Muskulatur gemessen. Zum Schluss musste nochmals 30 Minuten maximal belastet werden, wobei sich eine um 11% verbesserte Leistung (kJ) gegenüber vor der Supplementierung und um 35% gegenüber der Kontrollgruppe ergab.
Dies sind sehr beeindruckende Resultate. Dennoch ist bei der sehr langen Supplementierung zu berücksichtigen, dass 2 x 80 g Kohlenhydrate täglich 640 kcal entsprechen, und dies je nach Energiebedarf in der Ernährung einberechnet werden muss, um nicht zu einer Gewichtszunahme zu führen. Tatsächlich stieg das Körpergewicht bei den sieben Athleten der Kontrollgruppe um durchschnittlich 2,4 kg an, während es bei der Carnitin-Gruppe unverändert blieb. Ob Carnitin eine Gewichtszunahme verhindern konnte, blieb angesichts der kleinen Testgruppe unklar.

Leistungssteigerung durch Carnitin erneut bestätigt
Eine Folgestudie (3) konnte dann belegen, dass bei identischem Einnahmeprotokoll (2 x täglich 80 g Kohlenhydrate plus 2 g L-Carnitintartrat) schon nach 12 Wochen um 20% erhöhte muskuläre Carnitinspeicher möglich sind. Erfreulicherweise wurde auch keine Gewichtszunahme festgestellt – ganz im Gegensatz zur Kontrollgruppe, welche dieselbe Kohlydratmenge aber ohne L-Carnitin einnahm. Diese legte nämlich im selben Zeitraum fast zwei Kilogramm an Fettmasse zu. Es scheint also, dass die früher befürchtete Gewichtszunahme (in Form von Fett) bedingt durch die (nötige) hohe Kohlehydrateinnahme nicht eintritt, wenn gleichzeitig mit L-Carnitin supplementiert wird.
Dass ein um 20% erhöhter Muskel-Carnitingehalt die Fettoxidation bei extensiven Ausdauerbelastungen verbessert ist aus früheren Studien bereits belegt. Neu wurde nun anhand von Gen-Analysen auch aufgezeigt, dass 73 von den 187 untersuchten, mit dem Energiestoffwechsel verknüpften Genen in der L-Carnitin Gruppe stärker bzw. in der Kontrollgruppe vermindert exprimiert wurden. Dies lässt auf einen insgesamt optimierten Fettstoffwechsel durch L-Carnitin schliessen.

Akute, vaskuläre Wirkung von L-Carnitin ohne Loading
An sich gibt es schon einige frühere Studien, welche eine klare Wirkung von L-Carnitin auch bei einer kurzzeitigen Supplementierung zeigten. Dies aber nicht im Zusammenhang mit erhöhtem muskulärem Carnitin, sondern offenbar aufgrund einer vaskulären Wirkung des im Blut zirkulierenden Carnitins. So gibt es einige Studien, welche nach körperlicher Belastung verminderten oxidativen Stress, erniedrigte Laktat-, Cortisol-, Creatinkinase- und Ammoniak-Werte bei L-Carnitin Gabe nachwiesen (4, 5). Je höher diese Stressparameter sind, desto länger dauert auch die Erholungsphase. Unter diesem Aspekt ist eine Supplementation in hohen Dosen auch relativ kurz vor einer sportlichen Aktivität durchaus empfehlenswert, da eine Erhöhung des muskulären Carnitingehalts dafür offenbar gar nicht nötig ist. Die regenerationsfördernde Wirkung von L-Carnitin wird auch gemäss einem Gutachten der Medizinischen Fakultät der Universität Genf nicht einer Erhöhung des muskulären Carnitingehalts, sondern einer vaskulären Schutzwirkung des im Blutkreislauf zirkulierenden L-Carnitins zugeschrieben. Zirkulierendes L-Carnitin bewirke eine akute pharmakologische Schutzwirkung gegen oxidative Schädigungen im Bereich der Mikro-Blutgefässe. Es wurde allerdings ebenfalls ausgeführt, dass Dosierungen unter 1 g keinen Effekt nachweisen konnten. Mit den obig diskutierten beiden Studien eines Carnitin-Loadings kann nun aber auch eine Glycogeneinsparung und direkte Leistungssteigerung im Zusammenhang mit erhöhten muskulärem Carnitingehalt als realistisch und machbar gelten.

Schlussfolgerungen und Empfehlungen
Erhöhte Muskel-Carnitingehalte können also sowohl die aerobe Leistungsfähigkeit verbessern (Glycogeneinsparung, erhöhter Fettstoffwechsel) als auch bei intensiver Belastung die anaerobe Leistungsfähigkeit (verlangsamte Laktatakkumulation) und die Gesamtleistung erhöhen.
Problematisch ist immer noch das relativ lange Einnahmeprotokoll zusammen mit der nötigen, sehr hohen Kohlenhydratgabe. Eine solche Supplementierung ist deswegen nämlich nicht für jedermann geeignet, sondern muss im Einzelfall beurteilt und auch genau kontrolliert werden. In vielen Fällen dürfte eine kurzzeitige Carnitin-Einnahme daher sinnvoller und ausreichend sein. Die positiven Resultate von Kurzzeit-Studien mit L-Carnitin können offensichtlich nicht auf einer Erhöhung des muskulären Carnitingehalts beruhen, sondern auf der vaskulären Schutzwirkung des im Blutkreislauf zirkulierenden Carnitins.
Die meisten Studien wurden mit Carnitin-Gaben von 2-4 g/Tag durchgeführt. Für eine Erhöhung des muskulären Carnitingehalts scheint aber, wie oben diskutiert, eine tägliche Einnahme während mind. 12 Wochen von 2 x 2 g L-Carnitintartrat notwendig, kombiniert mit je 80 g Kohlehydraten. Als untere Grenze für eine vaskuläre Wirkung werden 1 g L-Carnitin/Tag genannt.
Eine einfache Einnahmemöglichkeit bieten Carnitin-Ampullen oder das auch in der Studie von (2) verwendete CarniPure®, ein reines L-Carntitintartrat. Da der maximale L-Carnitinspiegel im Blut nach 2 ½ bis 4 h gemessen wird, wäre theoretisch also in diesem Zeitraum ein maximaler Insulinwert wünschenswert, was mit hochglykämischen Kohlenhydratgaben (2 x 80 g) angestrebt werden kann. Es bietet sich die Möglichkeit, die Einnahme mit einer kohlehydrathaltigen Mahlzeit oder - trainingsbedingt sowieso verwendeten - Kohlenhydrat-Produkten (Sportgetränk, Regenerationsprodukt) zu kombinieren, um so nicht zusätzliche 160 g Kohlehydrate pro Tag einnehmen zu müssen. Dies ist speziell für Sportler empfehlenswert, welche auf ihr Gewicht achten, müssen. Alternativ kann aber mit dem Carboloader die nötige Kohlehydratmenge einfach, hoch konzentriert, mit wenig Volumen eingenommen werden.

Erhöhte Fettoxidation mit dem Ziel Gewichtsabnahme
An dieser Stelle soll noch ergänzt werden, dass wir bisher über eine erhöhte Fettoxidation zwecks Schonung der Glycogenreserven und somit verbesserter Ausdauerleistung bei Leistungssportlern diskutierten. Völlig verfehlt wäre es, L-Carnitin mit Carboloading als Massnahme zur Verbesserung des Fettstoffwechsels zwecks Gewichtsabnahme zu kombinieren! Eine Erhöhung des muskulären Carnitingehalts mit täglich zusätzlich 160 g Kohlehydrate erreichen zu wollen, würde auch bedeuten diese Extrakalorien anderswo wieder einsparen zu müssen. Zumindest dürfte in solchen Fällen nur sinnvoll sein, die Carnitineinnahme mit Mahlzeiten zu koppeln, anstatt zusätzliche Kohlehydrate einzunehmen. Dennoch ist zu beachten, dass bei einer Diät nicht die maximierte Fettverbrennung in den Muskelzellen, sondern eine allgemein und langfristig erhöhte Fettverbrennung zwecks Abbau von Depotfett das Ziel ist. Und eine ausbleibende Gewichtszunahme durch L-Carnitin (bei erhöhter Energiezufuhr) kann nicht ohne weiteres einem Depotfettabbau (bei gleichbleibender Energiezufuhr) gleichgesetzt werden. Es bleibt zu klären, ob erhöhte Muskel-Carnitinspeicher auch unter Ruhe eine erhöhte Fettoxidation bewirken und nicht nur unter moderater Belastung.
Die akute, vaskuläre Wirkung von L-Carnitin im Fettstoffwechsel wird nicht mit einer Anreicherung im Muskel, sondern einer Pufferfunktion in- und ausserhalb der Zelle begründet, was insgesamt die Nutzung von Fettsäuren zur Energiebereitstellung verbessert. Laut einigen Untersuchungen geht es aber primär um die Verhinderung eines Abfalls des Muskelgehalts, bzw. eines Aufrechterhalten (und nicht einer Erhöhung) des zirkulierenden (vaskulären) Carnitinspiegels (Prinzip «fliessendes Wasser im Schlauch»). Andererseits muss aber der Fettstoffwechsel durch körperliche Aktivität überhaupt erst soweit in Gang gebracht werden, dass der Puffereffekt von L-Carnitin wie beschrieben zum entscheidenden Faktor für eine erhöhte Fettverbrennung wird.
Es gibt also durchaus Argumente für eine akute (vaskuläre Wirkung) als auch für eine chronische (Muskel-Carnitinspeicher) Einnahme von L-Carnitin – sowohl für Ausdauersportler als auch zum Fettabbau. Die zusätzliche Kohlehydrateinnahme bei der chronischen Carnitineinnahme dürfte aber sicherlich nicht sinnvoll für Gewichts- und Fettabbau sein.

Wirkmechanismus von L-Carnitin im Fett- und Energiestoffwechsel
Der Fettsäurentransport wird häufig als die Hauptfunktion von L-Carnitin angesehen. Entscheidender scheint aber gemäss dieser Betrachtung die pH-Pufferung. L-Carnitin stabilisiert den pH ausserhalb der Zellen via Pufferung von Coenzym A (CoA) durch die Bildung von Acetyl-Carnitin. Damit wird eine Anhäufung von Acetyl-CoA verringert und so ein wichtiges Enzym (Pyruvatdehydrogenase) für den carnitinabhängigen Transport der Fettsäuren in die Mitochondrien (Verbrennungsort) aktiv gehalten. Innerhalb der Zelle ist für die Verbrennung der freien Fettsäuren im Mitochondrium die Menge an freiem CoA entscheidend. Wenn aus einer Fettsäure (z. B. C-18) dann 9 Acetyl-Einheiten werden (C-2), die alle ein freies CoA brauchen, um in den Krebszyklus zu gelangen, steigt der CoA-Bedarf im Mitochondrium dramatisch an. L-Carnitin kann vorübergehend auch diese C-2-Einheiten binden und die energieliefernden Prozesse aufrechterhalten, was die Oxidation von Fetten erhöhen kann.

Produktempfehlungen L-Carnitin
SPONSER® bietet verschiedene L-Carnitin-Produkte an:
• CARNIPURE: Nahrungsergänzung mit L-Carnitin in CarniPure-Qualität von Lonza für leistungsorientiere Ultra-Ausdauer-Athleten
• CARNITIN 1000 MINERALDRINK: Elektrolyt-Drink mit 1000 mg L-Carnitin pro Portion
• CARNITINE 1000: Trinkampulle mit L-Carnitin (1000 mg) plus Zink (3.8 mg) und Magnesium (75 mg)

In Verbindung stehende Artikel
zum Thema » Fettstoffwechsel
zum Thema » Gewichtsreduktion
zum Thema » Wissenschaft

Literatur
1) Stephens FB et al. (2006): Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol, 102(3):1065-70.
2) Wall BT et al. (2011): Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. J Physiol, 589(4):963-73.
3) Stephens FB et al. (2013): Skeletal muscle carnitine loading increases energy expenditure, modulates fuel metabolism gene networks and prevents body fat accumulation in humans. J Physiol, 591(18):4655-66.
4) Galloway SDR et al. (2004): Effect of 2 weeks supplementation with L-Carnitine-L-Tartrate on plasma ammonia response to exercise. Conference proceedings, FASEB.
5) Spiering BA et al. (2008): Effects of L-carnitine L-tartrate supplementation on muscle oxygenation responses to resistance exercise. J Strenght Cond Res, 22(4):1130-5.
O’Connor JE et al. (1990): New roles of Carnitine metabolism in ammonia cytotoxicity. Adv Exp Med Biol 272:183-195.

Autor: Remo Jutzeler
Leiter F&E SPONSER SPORT FOOD
Ing. Lebensmittelwissenschaften FH
MAS Nutrition & Health ETHZ