4
Nutritional supplement series Br J Sports Med 2011;45:1005–1007. doi:10.1136/bjsports-2011-090397 1005 1 Department of Physical Education, Campus Universitario de Tafira, Canary Island, Spain 2 Department of Sports Medicine, Justus-Liebig- University, Giessen, Germany 3 Department of Sports Nutrition, Australian Institute of Sport, Canberra, Australia 4 Performance Influencers Limited, London, UK 5 University of Oxford, Green Templeton College, Oxford, UK Correspondence to L M Castell, University of Oxford, Green Templeton College, Oxford OX2 6HG, UK; [email protected] Accepted 7 July 2011 A–Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part 24 J A Calbet, 1 F C Mooren, 2 L M Burke, 3 S J Stear, 4 L M Castell 5 INTRODUCTORY REMARKS In this issue, we deal with three compounds. One is a hormone involved in fat metabolism, while another is a mineral whose status may be altered by exercise. The fi nal is a fat that might be digested and metabolised more efficiently than our common dietary fat sources. LEPTIN JA Calbet Leptin is a hormone secreted primarily by adipo- cytes from the white adipose tissue in direct pro- portion to the amount of body fat present. Leptin plays a crucial role in the regulation of appetite, body fat mass, basal metabolic rate and gonadal function. 1 Congenital deficiency of leptin is rare, but causes morbid obesity which is normalised following leptin treatment. Circulating leptin levels change acutely in accordance with energy balance; leptin levels increase with food ingestion and reduce with prolonged exercise and fasting. When there is a severe acute negative energy bal- ance, serum leptin levels dramatically reduce by 60–80%, despite small changes in total fat mass. Preventing this reduction in leptin levels could attenuate hunger in dieting athletes, facilitating the adjustment of body mass to specific targets. Nevertheless, there is no account of leptin misuse by athletes for this purpose. Leptin receptors are densely expressed in the cerebellum, even more so than in the hypothala- mus where leptin is supposed to exert its main action. Leptin-related changes owing to physical activity levels may promote structural changes in the cerebellum, which is strongly implicated in motor control and learning. Leptin receptors are also expressed in human skeletal muscle, 2 3 and more abundantly in women than men. 3 Here, the main action of leptin is believed to be the stimula- tion of fatty acid oxidation via several pathways. 4 Interestingly, these pathways are also activated 30 min after sprint exercise 5 and, like sprint exer- cise, leptin induces PGC1α expression and mito- chondrial biogenesis. It is known that exercise reduces leptin resistance in obese rodents or in rodents fed with high fat diets (which causes skel- etal muscle insulin and leptin resistance). However, little is known about the influence of exercise on the regulation of leptin receptors and leptin signal- ling in human skeletal muscle. In obese humans, leptin receptors are reduced in the vastus lateralis, 6 perhaps by a mechanism related to reduced physi- cal activity. By contrast, 12 weeks’ of weightlifting combined with endurance training does not seem to induce changes in the number of leptin receptors in the vastus lateralis of healthy men. 7 However, professional tennis players have increased expres- sion of leptin receptors in the triceps brachi of the dominant arm compared with the non-dominant arm. This suggests that chronic loading may regu- late the expression of leptin receptors in human skeletal muscle. 8 An increased expression of leptin receptors in overloaded skeletal muscle may facilitate muscle growth by a mechanism involving leptin signalling, either by leptin itself or by insulin like growth factor 1. In fact, leptin administration in mice with a congenital leptin deficiency (ob/ ob mice) promotes muscle hypertrophy. 9 Thus, hypothetically, athletes could think of using lep- tin or leptin agonists to facilitate a reduction of fat mass, control hunger, promote muscle signal- ling similar to that induced by sprint training and stimulate mitochondrial biogenesis, as well as using it as an anabolic agent when combined with strength training. Therefore, the concerned authorities should keep track of potential misuse of leptin or leptin agonists. MAGNESIUM FC Mooren Magnesium (Mg) is an essential biological element that is predominantly located in bones (approx 52%), muscle cells (28%), soft tissue (19%), serum (0.3%; concentration range 0.75–1.1 mmol/l) and red blood corpuscles (0.5%). Important food sources of Mg include vegetables, fish, nuts and whole grains. Serum acts as a transit pathway between bone stores and actively metabolising tissues and is not representative of the body’s Mg status. Intracellular Mg is under hormonal control in some cell types and regulated by a secondary active transport system, the Na + -Mg 2+ -exchanger. In both extra- and intracellular compartments, the equilibrium between ionised Mg 2+ and bound Mg is established. Only Mg 2+ is available to react in physiological and biochemical processes during cellular homeostasis by binding to organic sub- stances such as proteins, nucleic acids and nucle- otides. In general, Mg 2+ is an important regulator of three main complexes (1) enzyme activation, for example during energy metabolism; (2) stabi- lising membrane function and integrity; and (3) cell signalling, for example, intracellular calcium signals. 10 There is interest in the effect of exercise on magnesium status. 11 Acute exercise induces hypomagnesaemia (10 out of 18 studies) while group.bmj.com on December 8, 2014 - Published by http://bjsm.bmj.com/ Downloaded from

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Page 1: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part 24

Nutritional supplement series

Br J Sports Med 2011;45:1005–1007. doi:10.1136/bjsports-2011-090397 1005

1Department of Physical Education, Campus Universitario de Tafi ra, Canary Island, Spain2Department of Sports Medicine, Justus-Liebig-University, Giessen, Germany3Department of Sports Nutrition, Australian Institute of Sport, Canberra, Australia4Performance Infl uencers Limited, London, UK5University of Oxford, Green Templeton College, Oxford, UK

Correspondence to L M Castell, University of Oxford, Green Templeton College, Oxford OX2 6HG, UK; [email protected]

Accepted 7 July 2011

A–Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part 24J A Calbet,1 F C Mooren,2 L M Burke,3 S J Stear,4 L M Castell5

INTRODUCTORY REMARKSIn this issue, we deal with three compounds. One is a hormone involved in fat metabolism, while another is a mineral whose status may be altered by exercise. The fi nal is a fat that might be digested and metabolised more effi ciently than our common dietary fat sources.

LEPTINJA CalbetLeptin is a hormone secreted primarily by adipo-cytes from the white adipose tissue in direct pro-portion to the amount of body fat present. Leptin plays a crucial role in the regulation of appetite, body fat mass, basal metabolic rate and gonadal function.1 Congenital defi ciency of leptin is rare, but causes morbid obesity which is normalised following leptin treatment. Circulating leptin levels change acutely in accordance with energy balance; leptin levels increase with food ingestion and reduce with prolonged exercise and fasting. When there is a severe acute negative energy bal-ance, serum leptin levels dramatically reduce by 60–80%, despite small changes in total fat mass. Preventing this reduction in leptin levels could attenuate hunger in dieting athletes, facilitating the adjustment of body mass to specifi c targets. Nevertheless, there is no account of leptin misuse by athletes for this purpose.

Leptin receptors are densely expressed in the cerebellum, even more so than in the hypothala-mus where leptin is supposed to exert its main action. Leptin-related changes owing to physical activity levels may promote structural changes in the cerebellum, which is strongly implicated in motor control and learning. Leptin receptors are also expressed in human skeletal muscle,2 3 and more abundantly in women than men.3 Here, the main action of leptin is believed to be the stimula-tion of fatty acid oxidation via several pathways.4 Interestingly, these pathways are also activated 30 min after sprint exercise5 and, like sprint exer-cise, leptin induces PGC1α expression and mito-chondrial biogenesis. It is known that exercise reduces leptin resistance in obese rodents or in rodents fed with high fat diets (which causes skel-etal muscle insulin and leptin resistance). However, little is known about the infl uence of exercise on the regulation of leptin receptors and leptin signal-ling in human skeletal muscle. In obese humans, leptin receptors are reduced in the vastus lateralis,6 perhaps by a mechanism related to reduced physi-cal activity. By contrast, 12 weeks’ of weightlifting combined with endurance training does not seem

to induce changes in the number of leptin receptors in the vastus lateralis of healthy men.7 However, professional tennis players have increased expres-sion of leptin receptors in the triceps brachi of the dominant arm compared with the non-dominant arm. This suggests that chronic loading may regu-late the expression of leptin receptors in human skeletal muscle.8

An increased expression of leptin receptors in overloaded skeletal muscle may facilitate muscle growth by a mechanism involving leptin signalling, either by leptin itself or by insulin like growth factor 1. In fact, leptin administration in mice with a congenital leptin defi ciency (ob/ ob mice) promotes muscle hypertrophy.9 Thus, hypothetically, athletes could think of using lep-tin or leptin agonists to facilitate a reduction of fat mass, control hunger, promote muscle signal-ling similar to that induced by sprint training and stimulate mitochondrial biogenesis, as well as using it as an anabolic agent when combined with strength training. Therefore, the concerned authorities should keep track of potential misuse of leptin or leptin agonists.

MAGNESIUMFC MoorenMagnesium (Mg) is an essential biological element that is predominantly located in bones (approx 52%), muscle cells (28%), soft tissue (19%), serum (0.3%; concentration range 0.75–1.1 mmol/l) and red blood corpuscles (0.5%). Important food sources of Mg include vegetables, fi sh, nuts and whole grains. Serum acts as a transit pathway between bone stores and actively metabolising tissues and is not representative of the body’s Mg status. Intracellular Mg is under hormonal control in some cell types and regulated by a secondary active transport system, the Na+-Mg2+-exchanger. In both extra- and intracellular compartments, the equilibrium between ionised Mg2+ and bound Mg is established. Only Mg2+ is available to react in physiological and biochemical processes during cellular homeostasis by binding to organic sub-stances such as proteins, nucleic acids and nucle-otides. In general, Mg2+ is an important regulator of three main complexes (1) enzyme activation, for example during energy metabolism; (2) stabi-lising membrane function and integrity; and (3) cell signalling, for example, intracellular calcium signals.10

There is interest in the effect of exercise on magnesium status.11 Acute exercise induces hypomagnesaemia (10 out of 18 studies) while

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Page 2: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part 24

Nutritional supplement series

Br J Sports Med 2011;45:1005–1007. doi:10.1136/bjsports-2011-0903971006

total intracellular Mg ([Mg]i) content of blood cells seems to be unchanged (7 out of 12 studies).Ionised [Mg2+]e was seen to decrease after high-intensity exercise while ionised [Mg2+]i increased.11 Results from animal studies suggest that Mg2+ is shifted from plasma into muscle and adipose tissue.12 Meanwhile, longitudinal and cross-sectional studies suggest that chronic exercise training may be followed by Mg2+ deple-tion and that athletes are prone to Mg2+ defi ciency; this is most likely due to Mg losses in sweat and urine. Dietary restric-tions, especially in athletes participating in sports requiring weight control, may aggravate the situation. One study has reported depleted Mg2+ status in a group of athletes compared with a control group, as indicated by enhanced retention of an intravenous dose of Mg2+ during a Mg2+ loading test.13 Mg2+

defi ciency is characterised by an enhanced neuromuscular excitability, including symptoms such as cardiac arrhyth-mias, headache, nervousness, and cramps of both smooth and skeletal muscle. The latter, however, have to be differentiated from exercise induced muscle cramps for which Mg supple-mentation has not been proven to be effective for so far.

A recent review14 indicates no signifi cant effect of Mg sup-plementation on exercise performance; this is the case for ath-letes with balanced Mg status, although single studies indicate that Mg supplementation may improve exercise economy (lower VO2max values at given intensity; better lactate clear-ance). However, Mg supplementation should be considered in athletes with Mg defi ciency based on fi ndings from animal experiments and in humans which suggest that magnesium defi ciency can compromise exercise capacity.

Magnesium supplements include both inorganic and organic compounds of which the latter seemed to have a better bio-availability. A range between 350 and 400 mg/day is recom-mended as the upper limit. In the case of individuals with renal insuffi ciency, the daily dose will need to be reduced. Common side effects include gastrointestinal problems such as nausea and diarrhoea. Intravenous application may cause hypotension and cardiac arrhythmias.15

MEDIUM-CHAIN TRIGLYCERIDESL M BurkeMedium-chain triglycerides (MCTs) are fats in which the fatty acids joined to the glycerol backbone are 6–14 carbon molecules in length. These fats are digested and metabolised differently from the long-chain fatty acids that make up most of our dietary fat intake. Specifi cally, MCTs can be digested within the intestinal lumen with less need for bile and pan-creatic juices than long-chain triglycerides, with the liberated medium chain fatty acids (MCFAs) being absorbed via the por-tal circulation. MCFAs are then taken up into the mitochon-dria without the need for carnitine-assisted transport. MCT supplements derived from palm kernel and coconut oil are used in clinical nutrition situations as an energy source for patients who have various digestive or lipid metabolism disorders.

Sports related applications of MCTs includes their use by body builders as an easily absorbed and oxidized fuel source that is less likely to deposit as body fat. There has been little investigation of such chronic use apart from some evidence that it may be associated with deterioration in blood lipid profi les.16 The best studied use of MCTs by athletes is as a source of rapidly accessible fat that can be consumed during exercise to increase fat availability during endurance and ultra- endurance events. In such events, there is both time to con-sume a fat source and the potential benefi ts if this leads to a

sparing of muscle glycogen use. The maximum rate of oxida-tion of MCTs occurs after about 120–180 min of exercise and co-ingestion with carbohydrate can increase this rate, possibly by increasing the rate of MCT absorption.17 The literature on supplementation with MCT and carbohydrate during ultra-endurance exercise is inconsistent, with the results appearing to depend on the amount of MCT that can be ingested and the prevailing hormonal conditions. Studies in which the intake of large amounts of MCT raised plasma free fatty acid concentra-tions and allowed glycogen sparing reported enhancement of a performance trial undertaken at the end of prolonged exer-cise.18 However, these metabolic (and performance) benefi ts may be compromised when exercise is commenced with higher insulin levels, as is the case following a carbohydrate-rich pre- exercise meal.19 20 The effectiveness of MCT is mostly limited by the inability of subjects to tolerate the substantial amount of MCT oils required to have a metabolic impact. A total intake of ~30 g appears to be the limit of gastrointestinal tolerance of MCT, which would limit its fuel contribution to 3–7% of the total energy expenditure during typical ultra-endurance events.17 Gastrointestinal reactions to larger intakes range from insignifi cant18 to performance-limiting.19 Differences in gas-trointestinal tolerance between or within studies may refl ect differences in the type and intensity of exercise, the mean chain length of MCTs found in the supplements or increased tolerance in some athletes due to chronic exposure to MCTs. Despite some support for use during prolonged exercise, MCTs appear to have limited application to most sporting situations.

CONCLUDING COMMENTSLeptin is a hormone of interest but there is currently insuf-fi cient knowledge to exploit how it or its agonists might con-tribute to performance of sport. Magnesium status may be altered by exercise, but there is no evidence of the benefi ts of magnesium supplementation unless it is used to treat an athlete with magnesium defi ciency. Finally, although there is a hypothetical opportunity to use MCTs as a fuel source for lengthy exercise tasks, the available evidence shows that the theoretical metabolic benefi ts are outweighed by the gastroin-testinal distress associated with the use of this supplement.

Competing interests F C Mooren received grants from Verla-Pharm Arzneimittel GmbH & Co. KG, 82327 Tutzing and Hermes Arzneimittel GmbH, 82049 Großhesselohe, Germany.

Provenance and peer review Commissioned; not externally peer reviewed.

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Br J Sports Med 2011;45:1005–1007. doi:10.1136/bjsports-2011-090397 1007

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part 24ergogenic aids for health and performance:supplements, sports nutrition foods and

Z of nutritional supplements: dietary−A

J A Calbet, F C Mooren, L M Burke, S J Stear and L M Castell

doi: 10.1136/bjsports-2011-0903972011 45: 1005-1007 Br J Sports Med 

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