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Current popular ergogenic aids used in sports: a critical review. (Review Paper).

Abstract

Many athletes make extensive use of ergogenic aids in the hope that they can favourably affect athletic performance and increase lean body mass. Supplementation with creatine, glutamine, camitine, leucine and its metabolite hydroxymethylbutyrate (HMB), and branched chain amino acids (BCAA) has been hypothesised to assist in the achievement of optimal sports performance. Despite an increasing amount of scientific evidence and popularity, uncertainty about the effectiveness and safety of these supplements still exists.

A survey was undertaken of the supplements being promoted in the most popular sports magazines in Australia. Approximately one quarter of the advertisements for supplements in the magazines surveyed were for creatine (54%), glutamine (24%), HMB (20%), and BCAA (2%). A critical literature review of trials of the effect of these ergogenic aids on exercise performance trials was conducted. Creatine supplementation appears to have substantial scientific support as a safe and effective nutritional strategy to enhance exercise performance and improve training adaptations in high-intensity, short-term ([less than or equal to] 30 seconds) exercise tasks, with limited recovery time between repetitions. Carnitine supplementation has been reported to increase exercise capacity in disease states. However, in healthy athletes carnitine was not shown to have an ergogenic effect. There was limited evidence that the use of HMB supplementation resulted in gains in strength and body mass. There was an abundance of clinical evi dence supporting the requirement for exogenous glutamine in critically ill patients and in the over-training syndrome. However, for healthy subjects, the few scientific studies available suggested that glutamine is only of benefit for athletes with true deficiency. Research findings regarding the effects of BCAA supplementation are somewhat equivocal. Most reviews evaluating the central fatigue hypothesis suggest that BCAA is not an effective ergogenic supplement, nor is it ergolytic. Further research is needed for better evaluation of the safety and efficacy of many of these supplements, especially focussing on their use in specific sporting situations.

Key words: ergogenic aids, hydroxymethylbutyrate, branched chain amino acids, creatine, carnitine, glutamine, sport nutrition, exercise

Introduction

The provision of sports supplements has become a multimillion dollar business and in popular sports magazines (such as Muscular Development, Iron Man, Muscles Magazine Flex, Muscle and Fitness, Muscle Media), creatine, glutamine, hydroxymethylbutyrate (HMB) and branched chain amino acids (BCAA) are among the most promoted supplements.

The process of substantiating the performance benefits or outcomes from nutrient supplementation is difficult. Under specific conditions ergogenic aids can have some positive effects on performance, lean body mass, strength and changes in body composition. Unfortunately there is often inadequate experimental evidence of efficacy or what exists is of poor quality. For some supplements there are sound trials demonstrating efficacy in the laboratory setting but not in the sports setting (1).

The following considerations are relevant when studying the effectiveness of specific sports ergogenic aids:

(1) In appropriate subject population; subjects should be highly trained in the specific sport performance factors that theoretically are enhanced by use of the sports ergogenic. If the sports ergogenic is effective, it should improve performance beyond the effects of training. Highly trained aerobic athletes, such as marathon runners or road cyclists, should serve as subjects, so that the variability in performance measures can be minimised;

(2) the performance tests used should be valid and reliable. Both laboratory (well-controlled) and field (real-world conditions) tests provide valuable information. Subjects should undertake a learning trial or trials to become proficient in the tests; the treatment should be based on sound theoretical rationale;

(3) an appropriate placebo should be used. The best design involves repeated-measures, crossover approach in which each subject randomly takes both the treatment and placebo, with an appropriate washout period between, and a double-blind protocol;

(4) investigators attempt to control extraneous factors and control the test environment that might influence test performance. During the conduct of the study, the athletes should maintain normal dietary and exercise training habits. Factors such as the exact composition and amount of an amino acid, the amount per serving and timing of ingestion in relation to the exercise may all influence study outcome (2);

(5) appropriate statistical techniques should be used to minimise the chance of statistical error (1) and how best to examine the data genreated by the studies (3). It must be considered whether statistical tests will detect the very small differences that can enhance performance.

Methods

A comprehensive literature review was conducted to find studies that examined the relationship between sports or ergogenic supplementation and changes in performance, strength and any other physiological metabolic response. The following databases were searched: MEDLINE (1996 to Week 3 September 2001, whole file), ProQuest 5000, American Physiological Society, Sprunger, SwetsNet Navigator and High Wire Press. Information about study design, method, sample size, subject characteristics, dose-effect and study outcomes published in peer-reviewed journals were summarised. Given the limited number of studies found and the heterogeneity of study design and characteristics, discussion of each supplement was conducted using the most credible evidence available to build a critical review of the state of the science at the current time. Assessment of quality and content was undertaken by the author. Information about study design, method, sample size, subject characteristics, dose-effect and study outcomes were conside red.

Results and discussion

Creatine

Creatine is a naturally occurring amino acid derived from the amino acids glycine, arginine, and methionine. Most creatine is stored in skeletal muscle, primarily as phosphocreatine; the remainder is found in the heart, brain, and testes (4,5). The daily creatine requirement is approximately two to three grams; half is obtained from diet, primarily from meat (500 g of uncooked steak contains about two grams of creatine) (6) and fish, while the remainder is synthesised (7). The amount of phosphocreatme in the skeletal muscle partially determines the length of time that maximum muscle work can be done (8). In theory, an increased store of creatine or phosphocreatine could improve the ability to produce energy during high-intensity exercise as well as improve the speed of recovery from high-intensity exercise (9). Creatine may also independently result in increased body mass (10), although in the first few weeks much of this increase may be due to increased water retention (8). Its use as a supplement to enhance sport performance has not been prohibited by the International Olympic Committee (8). Nevertheless, the US Food and Drug Administration recently warned consumers to consult a health professional before using creatine, and bodies such as the American College of Sports Medicine have taken a cautious view on the benefits and side effects of nutritional ergogenics aids (14). The safety of prolonged creatine supplementation has not been established, however, short-term supplementation (up to eight weeks) has not been associated with major health risks (3,6). Whether there are side effects from long-term use of creatine, particularly with high doses associated with rapid loading, remains to be determined. Some undocumented anecdotal reports indicate creatine supplementation may lead to muscle cramps, nausea, gastrointestinal upset, headache and possible muscle strains (3,6).

Table 1 shows the results of 35 studies on creatine supplementation. Most studies were undertaken using an experimental design, using a placebo control with the subjects supplemented with creatine at 0 to 25 g per day. In only one study subjects were administered 40 g of creatine per day (12). The creatine trials were from three days to 11 weeks in duration and included both healthy males and females, elite and untrained subjects (in the specific sport performance factors), active and sedentary participants. Of 35 studies ten did not find any significant effect of creatine supplementation on metabolism, performance or strength, nor any ergogenic effects or changes in body composition (13-22).

High-intensity ergometer protocols

In six studies using exercise tests ranging in duration from six to 30 seconds, the creatine group experienced a significantly lower decrease in performance compared to the placebo group (23-29). However, in four studies the investigators reported that creatine supplements produced no significant differences in peak or maximum power, time to exhaustion, performance or any other work measure (13,14,18,19). These more recent studies support the review by Williams (1) of 17 earlier studies, using cycle ergometer performance in a laboratory setting, 11 of which reported an ergogenic effect of creatine. Four of the 11 studies using cycle ergometer test summarised in Table 1 did not find improvements in the groups supplemented with creatine. In three of these studies the reason for the lack of effect may be that subjects were untrained (13,18,19) and in the other study a possible explanation for the negative result could be the cycle ergometry test, because the maximal performance was evaluated in a single test (a single ten-second test), one prior to and the other following, the supplementation period (14). Creatine is not usually considered ergogenic for single-bout or first-bout of exercise, because the likely benefit is too small to be detected (3).

Isokinetic protocols

Recent trials investigating the influence of creatine on isokinetic torque (elbow flexion) did not find significant effects (16,21), but earlier studies in the laboratory setting have shown that supplementation with 20 to 40 g per day for four to seven days may improve isokinetic torque force production and attenuate the decline in power during repetitive isokinetic exercise (6).

Isometric and resistance exercise protocols

Studies of the effect of creatine supplementation on isometric (knee extension, handgrip, elbow flexion) and resistance exercise tests (bench press, squat strength/jump, peak force and peak power) indicate changes in muscle ATP cost of contraction for isometric exercise (12,22). Only two of nine studies (12,22) failed to find this. Both studies used small sample sizes (nine subjects), and in one study the subjects differed in gender (six females and three males) and were not randomised (22). Also, because the sample size was small, it was possible that the study groups had different proportions of non-responders to creatine. Across studies there is evidence that the creatine-loading response varies between individuals, with approximately 30 % of individuals being 'non-responders' or failing to significantly increase muscle creatine stores (3,30). Ideally, studies employing large sample sizes and co-variant analysis should be used. This approach allows real changes to be detected and may also identify the char acteristics of individuals that predict 'response' and 'non-response' (3). Measurement of creatine stores in muscle (e.g. using magnetic resonance spectroscopy, a non-invasive method) is another way to determine if a person has responded with increases in muscle creatine after supplementation (31,32).

Sport performance protocols

Five studies have investigated the effect of creatine supplementation on actual sport performance (sprint running and swimming in a field setting), using high-intensity, short-duration repetitive activities (14,15,20,33,34). The outcomes were unanimous--finding no effect of creatine supplementation on performance. In one study, an increase in body mass occurred but there were no significant performance changes (33). More investigations are needed concerning the use of creatine in sports events involving multiple high-intensity, intermittent exercise tasks, such as soccer. In two studies of running performance creatine supplementation failed to improve run time (15,17). However, Harris et al. (35) also tested creatine supplementation and running performance, and it was found that the group that received supplementation (30 g of creatine for six days), showed enhanced performance in the final run and best time over 300 M. The authors suggested the increased use of phosphocreatine during exercise may contribute to the buffering of hydrogen ions (35). As has been found in laboratory studies, creatine supplementation does not appear to enhance performance in field studies involving more prolonged high-intensity tasks. Four of five field studies involving swimming and running performance, all using a double-blind placebo design, reported negative findings concerning the efficacy of creatine supplementation (1).

Factors influencing creatine supplementation

Dietary background may have a significant effect in creatine supplementation studies. Co-ingestion of substantial amounts of carbohydrate (57 to 100 g) with creatine doses has been shown to enhance creatine accumulation (36,37). The amount of carbohydrate that induces alterations on creatine loading is still under investigation but researchers should ensure adequate carbohydrate when studying the effects of supplementary creatine. Vegetarians do not consume a source of creatine and may demonstrate reduced body creatine stores, suggesting they do not totally compensate for the lack of dietary intake (38). It has been hypothesised that a high dosage of caffeine (5 mg per kg per day) counteracts the ergogenic effect of creatine supplementation (12,39) but there is some evidence that caffeine (in the quantities commonly found in food and beverages) does not interfere with creatine loading (40). Supplementation with caffeine (5 mg per kg per day) does not alter creatine-induced improvements in repeated high-intens ity exercise (41), maximal torque and contraction time in humans (42). A range of exercise activities may benefit from caffeine supplementation (3).

Summary

Creatine supplementation appears to be most effective in enhancing repetitive short-duration ([less than or equal to] 30 seconds), high-intensity tasks such as cycle ergometry; strength, torque and force production; and jump performance in a laboratory setting. In general, creatine supplementation has not been shown consistently to enhance performance in exercise tasks dependent on the lactic acid energy system (anaerobic glycolysis). Additionally, creatine supplementation has not been shown to enhance performance in aerobic endurance exercise tasks. More research is indicated, particularly on the effect of chronic supplementation as an aid to improving performance in competitive sport and of lower intensity activity, such as those performed by non-athletes in daily gym activities.

Hydroxymethylbutyrate (HMB)

The leucine metabolite hydroxymethylbutyrate (HMB) is found in some foods in small amounts (catfish and some citrus fruits), it is found in breast milk, and it is used and produced by body tissues (8). It has recently become a popular dietary supplement purported to promote gains in fat free mass and strength during resistance training (9). The rationale is that leucine and its metabolite [alpha]-ketoisocaproate appear to inhibit protein degradation (59,60) and this anti-proteolytic effect may be mediated by HMB. Although it seems that HMB has some influence on protein metabolism, the mechanisms behind any effects are unknown. It may regulate protein synthesis either through hormonal receptor effects (cortisol, testosterone, GH, IGF-1, insulin) or by modulating the enzymes responsible for muscle tissue breakdown. Hydroxymethylbutyrate may have effects on the metabolism of leucine and glutamine and perhaps other anabolic and anticatabolic amino acids, or may decrease gluconeogenesis and the subsequent oxidatio n of amino acids in the intracellular amino acid pool and catabolism of skeletal muscle cellular protein (8). It appears to be nontoxic (61,62).

Table 2 summarises data collected from eight studies (from 1996 to 2000) in which humans were fed 0 g, 3 g and/or 6 g HMB per day. The studies were from three to eight weeks' duration, included both males and females and healthy athletes or/and exercising subjects.

Of the eight studies only one found that HMB supplementation did not affect catabolism or induce changes in body composition and strength (63). This trial was not placebo-controlled and of short duration (28 days) and this may explain the lack of effect. Seven other studies on HMB supplementation have found significantly less exercise-induced proteolysis and muscle damage (64,65); increased strength and gains in fat free mass (64-66); or larger gains in muscle function and in resistance training (64,65). Only three studies (63,64) assessed exercise training in highly trained individuals and/or athletes. A recent study by S later et al. (68) reported HMB supplementation did not change strength or body composition in resistance-trained male athletes. It may be that further studies with highly trained individuals will find the impact of the supplements on exercise outcome are different to the earlier studies with less trained individuals (9).

All studies reported in Table 2 supplemented with 3 g of HMB per day. In two studies, 1.5 g of HMB per day was tested and compared with the results obtained with 3 g per day. Less effect was found for increase in strength and decrease of the exercise-induced proteolysis (64,65). Some other studies have compared 6 g HMB per day with 3 g per day, but doses of HMB higher than 3 g a day do not promote strength or gains in fat free mass (63-69). The popular use of supplemental HMB at 3 g per day for periods of up to one month (in a healthy population) as an ergogenic aid for exercise appears to be well-tolerated and safe in humans (62).

Summary

Given the generally good quality design of most of these studies, and the consistency of proven effects, it can be concluded that there is reasonable evidence that HMB supplementation results in gains in strength and body mass associated with resistance training, on enhancement of loss of body fat and on recovery from exercise (3). Although HMB supplementation during training may enhance training adaptations in untrained individuals initiating training, it is less clear whether HMB supplementation reduces markers of catabolism or promotes greater gains in fat free mass and strength during resistance training in well-trained athletes.

Glutamine

Glutamine provides nitrogen for the synthesis of nucleotides required in the formation of DNA and RNA during lymphocyte proliferation and macrophage activation (9). As glutamine is an important fuel for white blood cells, reductions in blood glutamine concentrations following intense exercise may contribute to immune suppression in overtrained athletes (70-73). Glutamine is utilised at a high rate by certain cells of the immune system (neutrophils, lymphocytes, and macrophages) and is essential for the viability and normal functioning of these cells (74,75). After prolonged intense exercise the number of lymphocytes in the blood is reduced, the function of natural killer cells is suppressed and secretory immunity is impaired (76). Glutamine has been demonstrated of benefit in trauma patients and individuals stressed by surgery (77,78). Although there are differences between exercising individuals and these patients, glutamine supplementation in athletes may be beneficial in increasing the anabolic drive (8). It has been theorised that a chronic glutamine debit may be responsible for the immunosuppression suffered by some athletes, and that supplementation may overcome the impaired immunity suffered by athletes undertaking repeated bouts of heavy training and overtraining (3). Regular runners are six times more likely to contract a cold virus in winter than nonparticipants (79). The few studies of increasing plasma glutamine concentrations with supplements have shown little or no effect on energy production or immune status (80,81). It is unclear whether long-term supplementation of glutamine affects protein synthesis, body composition, or the incidence of upper respiratory-tract infections during training (9).

The role of glutamine as an ergogenic aid has not been demonstrated in the scientific literature. Although there is evidence to support the requirement for exogenous glutamine in the maintenance of muscle protein mass and immune system function in the overtraining syndrome (77,78,82-84), little research has examined the use of glutamine for athletes (68). Blood glutamine concentrations may serve as a marker for determining whether athletes are overtraining (8,85). Studies have shown that decreased plasma glutamine concentrations are an objective, measurement of severe exercise stress and overtraining (86,87).

Summary

Few scientific data are available concerning potential benefits of glutamine supplementation for athletes. Further work is necessary to determine whether the benefits of exogenous glutamine supplementation shown in clinical situations apply in athletic populations. In those athletes demonstrating decreased plasma glutamine, supplements are indicated but this condition is uncommon.

Branched chain amino acids (BCAA)

The branched chain amino acids, valine, leucine and isoleucine, unlike most other amino acids, are oxidised by muscle cells, providing a source of cellular energy as ATP and phosphocreatine (7). There is a significant activation of BCAA metabolism with prolonged exercise, and studies indicate that this is more pronounced in endurance-trained subjects (88). Plasma concentrations of BCAAs are more affected by changes in energy, protein, fat, and carbohydrate intake in humans (89) than are the concentrations of other amino acids. Theoretically, BCAA supplementation (30% to 35% leucine) before and during endurance exercise may prevent or decrease the net rate of protein degradation, improve mental and physical performance and may have a sparing effect on muscle glycogen degradation and depletion of muscle glycogen stores (90). During intense training BCAA supplementation can help minimise protein degradation and thereby lead to greater gains in fat free mass (91-93), however, it can significantly increase plasma ammonia (toxic to the brain and muscle) (77) and lower physical performance in humans (94) and in rats (95). Reduced availability of BCAA has been theorised to contribute to central fatigue (79). During endurance exercise, BCAA are taken up by the muscles and the resultant decline in plasma BCAA can lead to an increase in the ratio of free tryptophan to BCAA, promoting the formation of the neurotransmitter 5-hydroxytryptamine (5-HT) in the brain. It has been shown to induce sleep, depress motor neuron excitability, influence autonomic and endocrine function, and suppress appetite in both humans and animals (93,96,97). An exercise-induced imbalance in the ratio of free tryptophan to BCAA has been implicated as a cause of acute physiological and psychological fatigue (the central fatigue) (93,96,97). The ingestion of carbohydrate during exercise minimises the unfavourable change in the ratio of plasma free tryptophan: BCAA (3,98).

Table 3 shows the results of nine studies on the effect of BCAA supplementation (from 1991 to 2001). The studies were undertaken using placebo-controlled designs and subjects were supplemented with up to 22 g of BCAA. The trials were short-term studies from a few hours to a day. Healthy males and females were used, including both trained and untrained subjects. Three of nine studies failed to find any significant effect of BCAA supplementation on metabolism and/or performance (99-101).

Performance-based endpoints (fatigue, work performed and mental performance)

Of four studies in which performance was considered the main and/or only outcome, three failed to show any benefit of BCAA supplementation (99-101). The one study that reported an increase in performance of a 'slower runners' group (85) has been criticised for its methodology (11). Mental performance was measured in three of the nine studies using the Stroop Colour Word Test, and in all three improvements were found (100,102,103).

Metabolic-based endpoints

Metabolic endpoints (ammonia accumulation and production, the tryptophan: BCAA ratio, amino acids and lactate production, protein breakdown) were tested in four studies (104-107) and improvements were found in all. However in the study of Blomstrand and Saltin (107) the anabolic effect on muscle protein metabolism may be significant only during recovery. The results observed during exercise were too variable to form any conclusion.

Carbohydrate is not only an energy source during exercise but may also have positive effects on amino acid metabolism (108) and nitrogen balance (109-112). The positive effects are likely due to an insulin-mediated stimulation of protein synthesis and an attenuation of protein breakdown (3). Supplementation with carbohydrate during exercise suppresses the rise in free fatty acids concentrations, thereby attenuating the increase in free tryptophan concentrations (98) that is an effective strategy against both peripheral and central mechanisms of fatigue (3). Thus, several investigators emphasise the importance of dietary carbohydrate before, during and between repeated bouts of prolonged exercise to minimise central fatigue (81,97,98,113,114).

Summary

Research findings regarding the effects of BCAA supplementation on endurance performance in humans do not offer substantial proof. Most other reviewers evaluating the central fatigue hypothesis have concluded overall there is not convincing evidence that supplementation with BCAA prevents or stimulates central fatigue (108,115-118). Studies comparing the intake of BCAA and carbohydrate with the supplementation of carbohydrate alone are necessary to determine if BCAA exert an independent effect.

Carnitine

Carnitine in humans is derived from both dietary sources and endogenous biosynthesis. Meat and dairy products are major dietary sources of this compound (119). According to Brass, a number of specific mechanisms have been postulated for an effect of carnitine on exercise performance including: enhanced muscle fatty acid oxidation; decreased rate of muscle glycogen depletion; shifts in substrate utilisation in muscle from fatty acid to glucose; activation of pyruvate dehydrogenase via lowering of acetyl-CoA; improved muscle fatigue resistance; and replacement of carnitine lost during training (120). If carnitine administration increases muscle fatty acid oxidation, this might also delay the use of muscle glycogen and thus delay fatigue development (121).

Table 4 shows the results of 11 studies on the effect of carnitine supplementation (1988 to 2000). Most studies involved oral supplementation with carnitine at 0 to 6 g per day but two studies used intravenous carnitine administration (122,123). The duration of trials ranged from one to 28 days, they included only healthy males, and used untrained, moderately-trained or highly-trained subjects. Three of the 11 studies found a significant effect of carnitine supplementation on performance plasma concentration of lactate and pyruvate, time to exhaustion or maximal oxygen consumption during exercise ([VO.sub.2max]) (124-126).

Performance-based protocols

Some studies in which exercise capacity was tested with use of [VO.sub.2max] and/or performance endpoints failed to show any benefit of carnitine supplementation (127,128). Similarly, studies searching for any ergogenic effect of carnitine supplementation during bouts of high-intensity anaerobic exercise in highly-trained subjects and during aerobic combined with anaerobic exercise failed to identify any improvement in metabolism, performance or lean body mass (122,129). However in one study, although no changes were found during exercise, an increase in fatty acid oxidation during recovery was observed (122).

Metabolic indices protocols

Most of the studies measuring metabolic indices of exercise (muscle fuel, muscle carnitine content, time to exhaustion, substrate utilisation, i.e. lipid or carbohydrate oxidation) failed to find any effect of carnitine administration (123,126,130-133). However Vecchiet et al. (128) found a decrease in lactate accumulation and/or production and Siliprandi et al. (125) reported a reduction in lactate and pyruvate. The latter study involved supplementation 60 or 90 minutes before exercise and it is difficult to discern if sufficient time elapsed for absorption and muscle uptake (125).

Although most studies demonstrate an increase in plasma carnitine concentrations following supplementation of I to 6 g carnitine per day, the effect on muscle carnitine content is less clear. The consensus is that there is no compelling evidence that the muscle content of carnitine is enhanced by supplementation (3,134,135). The few studies that report favourable metabolic outcomes, or an increase in exercise performance, are hard to explain. Hultman et al. (136) consider that it is unlikely that carnitine supplementation over a period of days to weeks will change total muscle carnitine content in humans. Available data confirm that muscle carnitine content is not increased by supplementation protocols similar to those described above (123,132,133), despite increases in plasma carnitine concentrations (120,122,123,129,132,133). Thus, although it is possible that camitine affects exercise physiology without modifying muscle carnitine poois, such a mechanism would clearly be distinct from the rationale usually made for supplementation. It is still possible that increases in muscle carnitine content might result from longer duration of therapy or/and muscle camitine homeostasis (120).

Only three studies provide evidence for a distinct effect of carnitine, the studies by Arenas et al. (126,137) and Huertas et al. (138). They examined only athletes engaged in training programs for periods of one to six months. Under these conditions, carnitine supplementation prevented a training-associated decrease in muscle carnitine content and also increased muscle activity of key oxidative enzymes, including pyruvate dehydrogenase and electron transport chain enzymes. The physiological effect of these changes is unknown and further corroboration of these findings is needed.

Summary

The data available to date do not allow a definitive conclusion concerning the effect of carnitine on exercise metabolism and performance. Most studies have design limitations and further research using placebo-controlled trials, with bigger sample sizes, and examining other relevant endpoints is indicated.

Conclusions

Table 5 summarises the supplementation studies reviewed, evaluating the strength of the ergogenic effect and the conditions under which each supplement is ergogenic.

Creatine is the most studied of the amino acid supplements. Creatine supplementation appears to be an effective nutritional strategy to enhance high-intensity exercise performance and improve training adaptations in high-intensity, short-term ([less than or equal to]30 seconds) exercise tasks, with limited recovery time between repetitions. No significant improvement in aerobic endurance exercise tasks is demonstrated. Further research in field settings is needed to study effects on intermittent activity. The safety of long-term supplementation requires further study, particularly with regard to large doses that are associated with rapid loading and unconfirmed side effects such as cramps, muscle tears and pulls.

A small number of recent well-designed studies of supplementation with HMB indicate that it results in gains in strength and body mass associated with resistance training, as well as enhanced loss of body fat and recovery from exercise in the healthy population. Whether the same outcomes would be found for highly-trained individuals is not clear and more research is needed.

There is an abundance of clinical evidence supporting the need for exogenous glutamine in critically ill patients for the maintenance of muscle protein mass and immune system function. However, for healthy subjects the few scientific results available suggest that glutamine is only of benefit for athletes who show a true deficiency. The overtrained may have lower glutamine plasma concentrations but it remains unclear whether supplementation improves their condition.

Research findings regarding the effects of BCAA supplementation are equivocal. Most reviews evaluating the central fatigue hypothesis suggest that BCAA is not an effective ergogenic supplement. The few data available do not allow a conclusive position regarding the effect of BCAA supplementation on exercise metabolism and performance and more studies are needed.

Carnitine supplementation has been reported to increase exercise capacity in disease states. However, in healthy athletes carnitine fails to provide a significant ergogenic effect. Moreover, the few study trials that reported favourable outcomes or an increase in exercise performance suffer from design limitations.

Further research is still needed for better evaluation of the safety and efficacy of many of these supplements, especially focussing on their use in specific sporting situations. The marketing of sport supplements is an international, multimillion dollar business that preys upon the desires of athletes to be the best. The most appropriate advice to athletes may be to avoid using a specific sport supplement until the product has been evaluated for safety, efficacy, potency and legality. Athletes should discuss the use of any supplement with a qualified sports nutritionist, dietitian, or health professional. All users and creators of supplement information should consult the sport policy of the Australian Institute of Sport (www.ais.org.au/nutrition)--under supplements.
Table 1

Summary of research studies on creatine supplementation in exercising,
trained or untrained individual, published 1996-2000 (n=35)

Study Subjects

High intensity ergometer protocols

Barnett et al. 1996 (13) 17M (active males)

Burke et al. 1996 (14) 32M/F (elite swimmers)

Casey et al. 1996 (23) 9M (healthy males)

Cooke & Barnes, 1997 (18) 80M

Kirksey et al. 1997 (25) 36M/F (track/field athletes)

Odland et al. 1997 (19) 9M (active but untrained

Prevost et al. 1997 (26) 18M/F (college students)

Schneider et al. 1997 (24) 9M (untrained males)

Smith et al. 1998 (27) 15M/F (untrained)

Vandenbuerie et al. 1998 (28) 12M (amateur cyclists)

Kamber et al. 1999 (29) 10M (trained sport students)


Isokinetic protocols

Vandenberghe et al. 1996a (16) 20F
Hamilton-Ward et al. 1997 (21) 20F (athletes)
Van Leemputte et al. 1999 (43) 16M (untrained)


Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) 9M (healthy males)

Becque et al. 1997 (44) 23M (weight-lifters)

Kurosawa et al. 1997 (45) 5M/F (healthy)

Vandenberghe et al. 1997a (46) 19F (healthy sedentary)

Volek et al. 1997 (47) 14M (healthy active)


Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) 10M (weight-trained)


Smith et al. 1999 (32) 9M/F (active-untrained)

Stone et al. 1999 (49) 42M (college football players)



Urbanski et al. 1999 (50) 10M (active-untrained)
 untrained)


Volek et al. 1999 (51) 19M (resistance-trained)



Burke et al. 2000 (52) 41M (university athletes





Sport performance protocols

Mujika et al. 1996 (33) 20M/F (elite swimmers)
 swimmers)
Redondo et al. 1996 (15) 18M/F (trained athletes)

Bosco et al. 1997 (53) 14M (sprinters & jumpers


Goldberg & Bechtel, 1997 (20) 34M (football/track athletes)
Grindstaff et al. 1997 (54) 18M/F (junior swimmers)

Terrillion et al. 1997 (17) 12M (competitive runners)

McNaughton et al. 1998 (55) 16 M (elite surf-ski/kayak)

Peyrebrune et al. 1998 (56) 14M (elite swimmers)

Leenders et al. 1999 (57) 32M/F (college swimmers)

Theodorou et al. 1999 (58) 22 M/F (clite swimmers)



Study Study type (a)

High intensity ergometer protocols

Barnett et al. 1996 (13) RDBPC

Burke et al. 1996 (14) RDBPC

Casey et al. 1996 (23) SGRM

Cooke & Barnes, 1997 (18) RPC

Kirksey et al. 1997 (25) RDBPC

Odland et al. 1997 (19) SGRM

Prevost et al. 1997 (26) RPC

Schneider et al. 1997 (24) RSBPC

Smith et al. 1998 (27) RDBPC

Vandenbuerie et al. 1998 (28) RDBPC

Kamber et al. 1999 (29) DBPCX


Isokinetic protocols

Vandenberghe et al. 1996a (16) RDBPC
Hamilton-Ward et al. 1997 (21) RDBPC
Van Leemputte et al. 1999 (43) DBPC


Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) RDBPCX

Becque et al. 1997 (44) DBPC

Kurosawa et al. 1997 (45) SGRM

Vandenberghe et al. 1997a (46) DBPC

Volek et al. 1997 (47) RDBPC


Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) RDBPCX


Smith et al. 1999 (32) SBPC

Stone et al. 1999 (49) RDBPC



Urbanski et al. 1999 (50) RDBPCX



Volek et al. 1999 (51) RDBPC



Burke et al. 2000 (52) RDBPC





Sport performance protocols

Mujika et al. 1996 (33) RDBPC

Redondo et al. 1996 (15) RDBPC

Bosco et al. 1997 (53) RBDPC


Goldberg & Bechtel, 1997 (20) RDBPC
Grindstaff et al. 1997 (54) RDBPC

Terrillion et al. 1997 (17) RDBPC

McNaughton et al. 1998 (55) RDBPCX

Peyrebrune et al. 1998 (56) RDBPC

Leenders et al. 1999 (57) RDBPC

Theodorou et al. 1999 (58) RPC



Study Creatine dose-trial

High intensity ergometer protocols

Barnett et al. 1996 (13) 20 g/day-4 days

Burke et al. 1996 (14) 20 g/day-5 days

Casey et al. 1996 (23) 20 g/day-5days

Cooke & Barnes, 1997 (18) 20 g/day-5days

Kirksey et al. 1997 (25) 0.3 g/kg/day-42 days

Odland et al. 1997 (19) 20 g/day-3 days

Prevost et al. 1997 (26) 18.75 g/day-5 days
 2.25 g/day-7days
Schneider et al. 1997 (24) 25 g/day-7 days

Smith et al. 1998 (27) 20 g/day-5 days

Vandenbuerie et al. 1998 (28) 25 g/day-4 days

Kamber et al. 1999 (29) 20 g/day-5 d (28 days trial)


Isokinetic protocols

Vandenberghe et al. 1996a (16) 20 g/day-4 days
Hamilton-Ward et al. 1997 (21) 25 g/day-7 days
Van Leemputte et al. 1999 (43) 20 g/day-5 days


Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) 40 g/day-6 days

Becque et al. 1997 (44) 20 g/day-7 days

Kurosawa et al. 1997 (45) 5 g/day-14 days

Vandenberghe et al. 1997a (46) 20 g and 5 g/day-10 weeks

Volek et al. 1997 (47) 25 g/day-7 days


Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) 10 g/day-5days


Smith et al. 1999 (32) 0.3 g/kg/day-5 days

Stone et al. 1999 (49) 0.22 g/kg/day-7 weeks



Urbanski et al. 1999 (50) 20 g/day-5 days



Volek et al. 1999 (51) 25 g/day-1 week &
 5 g/day-11 weeks


Burke et al. 2000 (52) 7.7 g/day-21 days





Sport performance protocols

Mujika et al. 1996 (33) 20 g/day-5 days

Redondo et al. 1996 (15) 25 g/day-7 days

Bosco et al. 1997 (53) 20 g/day-5 days


Goldberg & Bechtel, 1997 (20) 3 g/day-14 days
Grindstaff et al. 1997 (54) 21 g/day-9 days

Terrillion et al. 1997 (17) 20 g/day-5 days

McNaughton et al. 1998 (55) 20 g/day-5 days

Peyrebrune et al. 1998 (56) 9 g/day-5 days

Leenders et al. 1999 (57) 20 g/day-6 days

Theodorou et al. 1999 (58) 25 g/day-4 days



Study Event/Exercise test

High intensity ergometer protocols

Barnett et al. 1996 (13) Cycling (7 x 10 sec sprints)

Burke et al. 1996 (14) Leg ergometry (2 x 10 sec sprints)

Casey et al. 1996 (23) Cycling (2 x 30 sec sprints)

Cooke & Barnes, 1997 (18) Cycling (30, 60, 90, 120 sec of
 recovery)
Kirksey et al. 1997 (25) Cycling (Wingate test)

Odland et al. 1997 (19) Cycling (30 sec Wingate test)

Prevost et al. 1997 (26) Cycling (time exhaustion at 150%
 [VO.sub.2 max])
Schneider et al. 1997 (24) Cycling (5 x 15sec)

Smith et al. 1998 (27) Cycling (4 maximal bouts-
 ergonometer)
Vandenbuerie et al. 1998 (28) Cycling (progressive to exhaustion)

Kamber et al. 1999 (29) Cycling (10 x 6 sec, 30 sec rest)


Isokinetic protocols

Vandenberghe et al. 1996a (16) Isokinetic (5 x 30 max arm)
Hamilton-Ward et al. 1997 (21) Isokinetic (elbow flexion torque)
Van Leemputte et al. 1999 (43) Maximal isometric elbow-flexions on
 isokinetic dymometer

Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) Isometric and isokinetic (3 x max)

Becque et al. 1997 (44) Isotonic (bicep curl 1-repetition
 max)
Kurosawa et al. 1997 (45) Isometric (high intensity)

Vandenberghe et al. 1997a (46) Resistance training (3 hrs/week)

Volek et al. 1997 (47) Isotonic (jump squad 5 x 10
 repetition max)

Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) Knee extension (maximal and
 exhaustion)

Smith et al. 1999 (32) Leg knee extension to exhaustion

Stone et al. 1999 (49) Resistance exercise



Urbanski et al. 1999 (50) Maximal & submaximal isometric knee
 estension and handgrip exercise


Volek et al. 1999 (51) Resistance exercise (bench press,
 squat, strength/jump and
 muscular endurance)

Burke et al. 2000 (52) Bench press until exhaustion, peak
 force and peak power




Sport performance protocols

Mujika et al. 1996 (33) Swimming (25 m, 50 m and 100 m)

Redondo et al. 1996 (15) Running (3 x 60 m sprint)

Bosco et al. 1997 (53) Jumping and running and treadmill
 run

Goldberg & Bechtel, 1997 (20) Isotonic (1 repetition max bench)
Grindstaff et al. 1997 (54) Swimming (3 x 100 m freestyle
 sprint)
Terrillion et al. 1997 (17) Running (2 x maximal 700 m run)

McNaughton et al. 1998 (55) Kayaking (kayak ergonometer test)

Peyrebrune et al. 1998 (56) Swimming (maximal swims)

Leenders et al. 1999 (57) Swimming

Theodorou et al. 1999 (58) Swimming



Study Effect

High intensity ergometer protocols

Barnett et al. 1996 (13) No

Burke et al. 1996 (14) No

Casey et al. 1996 (23) Yes

Cooke & Barnes, 1997 (18) No

Kirksey et al. 1997 (25) Yes

Odland et al. 1997 (19) No

Prevost et al. 1997 (26) Yes

Schneider et al. 1997 (24) Yes

Smith et al. 1998 (27) Yes

Vandenbuerie et al. 1998 (28) Yes

Kamber et al. 1999 (29) Yes


Isokinetic protocols

Vandenberghe et al. 1996a (16) No
Hamilton-Ward et al. 1997 (21) No
Van Leemputte et al. 1999 (43) Yes


Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) Yes

Becque et al. 1997 (44) Yes

Kurosawa et al. 1997 (45) Yes

Vandenberghe et al. 1997a (46) Yes

Volek et al. 1997 (47) Yes


Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) Yes


Smith et al. 1999 (32) No

Stone et al. 1999 (49) Yes



Urbanski et al. 1999 (50) Yes



Volek et al. 1999 (51) Yes



Burke et al. 2000 (52) Yes





Sport performance protocols

Mujika et al. 1996 (33) Yes

Redondo et al. 1996 (15) No

Bosco et al. 1997 (53) Yes


Goldberg & Bechtel, 1997 (20) No
Grindstaff et al. 1997 (54) Yes

Terrillion et al. 1997 (17) No

McNaughton et al. 1998 (55) Yes

Peyrebrune et al. 1998 (56) Yes

Leenders et al. 1999 (57) Yes

Theodorou et al. 1999 (58) Yes



Study Comments

High intensity ergometer protocols

Barnett et al. 1996 (13) No effect on multiple cycle perform

Burke et al. 1996 (14) No significant effect on leg
 ergometry performance
Casey et al. 1996 (23) Increase in total work (1%) and
 peak power (4%)
Cooke & Barnes, 1997 (18) No effect on maximum power or peak
 power output
Kirksey et al. 1997 (25) Increase in mean peak power (13%)

Odland et al. 1997 (19) No effect on any recorded exercise
 measures
Prevost et al. 1997 (26) Significant increase was found for
 all work measures
Schneider et al. 1997 (24) Improved total work (6.5%) during
 bout of maximal cycling
Smith et al. 1998 (27) Improved time to exhaustion at
 shorter, higher-intensity exercise
Vandenbuerie et al. 1998 (28) Improved power output for the
 maximal sprints
Kamber et al. 1999 (29) Supplementation improved short-term
 performance, increased body mass

Isokinetic protocols

Vandenberghe et al. 1996a (16) No ergogenic effect
Hamilton-Ward et al. 1997 (21) No ergogenic effect was found
Van Leemputte et al. 1999 (43) Relaxation time reduced following
 creatine

Isometric, isotonic and resistance
 exercise protocols

Vandenberghe et al. 1996b (12) Increase in torque production, but
 no effect for isometric
Becque et al. 1997 (44) Increase in bicep curl (28%)

Kurosawa et al. 1997 (45) Ergogenic effect (20% untrained
 arm, 35% trained arm)
Vandenberghe et al. 1997a (46) Long-term supplementation enhances
 progress of muscle strength
Volek et al. 1997 (47) Significant increase in repetitions
 to exhaustion and peak power for
 squats. Increase in body mass
Isometric, isotonic and resistance
 exercise protocols

Maganaris & Maughan, 1998 (48) Increased maximum voluntary
 contraction, endurance capacity
 and body mass
Smith et al. 1999 (32) Muscle ATP cost of contraction
 not affected
Stone et al. 1999 (49) Increased squat and bench press,
 static vertical jump power output.
 Increase in body mass and lean
 body mass
Urbanski et al. 1999 (50) Increased maximal and submaximal
 knee-extension torque, handgrip
 exercise and time to fatigue. No
 significant increase in body mass
Volek et al. 1999 (51) Improved bench press and squat,
 increased muscle fibre cross-
 sectional areas. Increase in body
 mass and lean body mass
Burke et al. 2000 (52) Increased total work and great
 improvements in force and power
 peak. Improved factors associated
 with short-duration, high-
 intensity activity

Sport performance protocols

Mujika et al. 1996 (33) Increase in body mass but no
 significant performance changes
Redondo et al. 1996 (15) No significant difference between
 groups
Bosco et al. 1997 (53) Improved jumping performance of the
 jumping test and improved
 intensive running time exhaustion
Goldberg & Bechtel, 1997 (20) No ergogenic effect was found
Grindstaff et al. 1997 (54) Improved swim time

Terrillion et al. 1997 (17) No significant differences between
 placebo or supplemented
McNaughton et al. 1998 (55) Significant increase in work in all
 tests, increase in body mass
Peyrebrune et al. 1998 (56) Increased performance as there was
 a reduction in total sprint time
Leenders et al. 1999 (57) Mean overall swimming velocity
 improved. No change in body mass
Theodorou et al. 1999 (58) Improvement (1.5%) in mean swim and
 interval set. Increase in body
 mass

(a)RDBPC: randomised double-blind placebo control, RPC: randomised
placebo control, RSBPC: randomised single-blind placebo control, SGRM:
single group repeated measures; RDBPCX: randomised double-blind placebo
control crossover.

Table 2

Summary of the research studies on [beta]-hydroxy-[beta]-methylbutyrate
(HMB) supplementation in exercising (trained or untrained individuals),
conducted from 1996-2000 (n = 8)

 Study Subjects

Nissen et al. 1996a (65) n = 41M)
(Endurance-exercise) (healthy subjects


Nissen et al. 1996a (65) n = 28
(Resistance-training) (trained subjects)



Nissen et al. 1996b (64) n = 40M
(Resistance-training)



Kreider et al. 1999 (63) n = 40M (athletes)
(Resistance-training)



Kreider et al. 1999 (63) n = 41M (athletes)
(Resistance-training)



Knitter et al. 2000 (66) n = 13
(Resistance-training) (5M 8F)

Gallagher et al. 2000 (69) n = 37M
(Strength-training)





Panton et al. 2000 (67) n = 75
(Resistance-training) (39M 36F)




 Study Study type

Nissen et al. 1996a (65) Placebo-controlled, Randomised
(Endurance-exercise)


Nissen et al. 1996a (65) Placebo-controlled,
(Resistance-training) Single-blind, Randomised



Nissen et al. 1996b (64) Placebo-controlled, Randomised
(Resistance-training)



Kreider et al. 1999 (63) Double-blind, Randomised
(Resistance-training)



Kreider et al. 1999 (63) Double-blind,
(Resistance-training) Placebo-controlled, Randomised



Knitter et al. 2000 (66) Double-blind,
(Resistance-training) Placebo-controlled, Randomised

Gallagher et al. 2000 (69) Double-blind,
(Strength-training) Placebo-controlled, Randomised





Panton et al. 2000 (67) Double-blind,
(Resistance-training) Placebo-controlled, Randomised




 Study HMB dose-duration trial Effect

Nissen et al. 1996a (65) 1.5 g or 3 g/day - 3 wk trial Yes
(Endurance-exercise)


Nissen et al. 1996a (65) 3 g/day - 7 wk trial Yes
(Resistance-training)



Nissen et al. 1996b (64) 3 g/day - 4 wk trail Yes
(Resistance-training)



Kreider et al. 1999 (63) 3 g or 6 g/day - 28 days trial No
(Resistance-training)



Kreider et al. 1999 (63) 3 g or 6 g/day - 4 wk trial Yes
(Resistance-training)



Knitter et al. 2000 (66) 3 g/day - 8 wk trial Yes
(Resistance-training)

Gallagher et al. 2000 (69) 3 g or 6 g/day - 7 wk trial Yes
(Strength-training)





Panton et al. 2000 (67) 3 g/day - 4 wk trial Yes
(Resistance-training)




 Study Comments

Nissen et al. 1996a (65) HMB significantly decreased
(Endurance-exercise) the exercise-induced
 proteolysis and increase
 strength.
Nissen et al. 1996a (65) HMB prevented proteolysis and
(Resistance-training) muscle damage and results in
 larger gains in muscle
 function and in
 resistance-training.
Nissen et al. 1996b (64) HMB supplementation increased
(Resistance-training) bench press strength, fat
 free mass gain, but no effect
 on fat mass.

Kreider et al. 1999 (63) 28 d of HMB supplementation in
(Resistance-training) athletes does not reduce
 catabolism or induce changes
 in body composition and
 strength.
Kreider et al. 1999 (63) HMB supplementation promotes
(Resistance-training) no gains in body mass, fat
 free mass or fat mass, but
 trend for increase work output
 on sprint test.
Knitter et al. 2000 (66) HMB helps prevent
(Resistance-training) exercise-induced muscle
 damage.
Gallagher et al. 2000 (69) Higher doses of HMB (>3 g/d)
(Strength-training) do not promote strength or
 fat free mass gains, however 3
 g appears to increase peak of
 isometric and isokinetic
 torque values and fat free
 mass gains.
Panton et al. 2000 (67) HMB supplementation may
(Resistance-training) increase upper body strength
 and decrease muscle damage,
 regardless of gender and
 training status.

Table 3

Summary of research studies on branched chain amino acid (BCAA)
supplementation in exercising, trained or untrained individuals, from
1991-2001 (n = 9)

Study Subjects Study type (a)

Soccer player protocols

Blomstrand et al. 1991 (103) 6F (national DBPCX
 standard soccer-
 field-players)

Davis et al. 1999 (101) 8M and F (active) PCX






Runner protocols

Blomstrand & Newsholme, 26M (cross- RPC
1992 (102) country)
 32M (marathon
 runners)






Davis et al. 1999 (101) 8M and F (active) PCX





Krogh ergonseter protocols

MacLean et al. 1994 (104) 5M (healthy RPC (own
 subjects) control)




MacLean et al. 1996 (105) 5M (healthy RPC (own
 subjects) control)






Cyclist protocols

Madsen et al. 1996 (99) 9M (well-trained DBPCX
 cyclists)

Blomstrand et al. 1997 (100) 7M (trained RDBPCX
 cyclists)



Mittleman et al. 1998 (106) 7M and 6F (13 DBPCX
 subjects)
 (moderately
 trained)

Blomstrand & Saltin, 2001 (107) 7M (recreational PC
 cyclists)







Study Carnitine dose-trial (b)

Soccer player protocols

Blomstrand et al. 1991 (103) 6%CHO+7.5 g BCAA or
 6%CHO
 40%val+35%leu+25%ile

Davis et al. 1999 (101) CHO+7 g BCAA or CHO or placebo
 (before/during/after)





Runner protocols

Blomstrand & Newsholme, 7.5 g BCAA (cross-country) or
1992 (102) 12 g BCAA (marathon)
 50%val+35%leu+15%ile or
 5%CHO+BCAA (cross-country)
 40%val+35%leu+25%ile or
 6%CHO+BCAA (marathon)




Davis et al. 1999 (101) CHO+7 g BCAA or CHO or
 placebo (before/during/after)




Krogh ergonseter protocols

MacLean et al. 1994 (104) 77 mg/kg (~5.5 g, 2 x 38.5 mg/kg
 45 min and 20 min before test)
 30%val+44%leu+26%ile



MacLean et al. 1996 (105) 308 mg/kg (154, 77 mg/kg- 45 &
 20 min prior to test and
 77 mg/kg-5 min after starting the
 test ~22 g)
 30%val+44%leu+26%ile



Cyclist protocols

Madsen et al. 1996 (99) 3.5 L @ 5% glucose or 5%
 glucose + 18 g BCAA:
 50%val+35%leu+15% ile
Blomstrand et al. 1997 (100) 90 mg/kg (~6.5 g), 40% val+35%
 leu+25% ile



Mittleman et al. 1998 (106) 9.4 g F and 15.8 g M 54%
 leu+19% ile+ 27% val



Blomstrand & Saltin, 2001 (107) 100 mg/kg (~7 g) in 1.5 L 150 ml
 before and immediately before
 test, during and after test
 30%val+45%leu+25%ile





Study Event/Exercise test (c)

Soccer player protocols

Blomstrand et al. 1991 (103) Soccer match (2 games
 separated by one week) CWT
 given before (~2 h) and
 within the game
Davis et al. 1999 (101) Running--intermittent shuttle
 run until exhaustion





Runner protocols

Blomstrand & Newsholme, Run - 30 km cross-country race or
1992 (102) marathon
 Run time + CWT after cross-
 country run






Davis et al. 1999 (101) Running--intermittent shuttle run
 until exhaustion




Krogh ergonseter protocols

MacLean et al. 1994 (104) Krogh ergonseter modified for one-
 legged knee extensor. 60 min of
 dynamic knee extensor exercise
 ~71% of maximum work capacity


MacLean et al. 1996 (105) Krogh ergometer modified for one-
 legged knee extensor. 90 min of
 dynamic knee exercise ~64% of
 maximum workload




Cyclist protocols

Madsen et al. 1996 (99) Cycling 100 km time trial as fast
 as possible (own bikes) connected
 to a magnetic brake
Blomstrand et al. 1997 (100) Cycling 60 min @ ~70%[VO.sub.2max]
 + 20 min time trial. Stroop Colour
 Word Test after ride


Mittleman et al. 1998 (106) Cycling (ergometry) in the heat
 (34[degrees]C), time to exhaustion
 @ 40%[VO.sub.2max]


Blomstrand & Saltin, 2001 (107) Cycling 1 hour of ergometer cycle
 exercise and 2 hours of recovery
 period. Work rate ~164W ~75%
 [VO.sub.2max]





Study Effect

Soccer player protocols

Blomstrand et al. 1991 (103) Yes



Davis et al. 1999 (101) No






Runner protocols

Blomstrand & Newsholme, Yes
1992 (102)








Davis et al. 1999 (101) No





Krogh ergonseter protocols

MacLean et al. 1994 (104) Yes





MacLean et al. 1996 (105) Yes







Cyclist protocols

Madsen et al. 1996 (99) No


Blomstrand et al. 1997 (100) No




Mittleman et al. 1998 (106) Yes




Blomstrand & Saltin, 2001 (107) Yes








Study Comments

Soccer player protocols

Blomstrand et al. 1991 (103) Improvement in CWT after game
 with CHO+BCAA. No such effect
 was found when subjects took
 the placebo drink (CHO).
Davis et al. 1999 (101) No performance differences
 between (CHO or CHO+BCAA)
 trials. CHO and CHO+BCAA
 increased time to fatigue
 compared to placebo. No
 further enhancement with BCAA.

Runner protocols

Blomstrand & Newsholme, CWT performance improved in BCAA
1992 (102) trial after cross-country run.
 'Slower runners' in BCAA group
 (marathon) ran faster but no
 significant effect on performance
 in the 'faster runners' group.
 BCAA ingested during exercise might
 decrease the net rate of protein
 degradation in human skeletal
 muscle during exercise.
Davis et al. 1999 (101) No performance differences between
 (CHO or CHO+BCAA) trials. CHO
 and CHO+BCAA increased time to
 fatigue compared to placebo. No
 further enhancement with BCAA.

Krogh ergonseter protocols

MacLean et al. 1994 (104) BCC supplementation results in
 significantly greater muscle
 ammonia production during
 exercise. Increased results in
 decrease of muscle protein
 breakdown during exercise.
MacLean et al. 1996 (105) Long-term exercise+BCAA
 administration significantly
 increase muscle ammonia, alanine &
 glutamine production, as well as
 lower lactate production, than is
 observed without BCAA
 supplementation.

Cyclist protocols

Madsen et al. 1996 (99) No performance differences between
 trials. Plasma BCAA and ammonia
 levels higher with BCAA trial.
Blomstrand et al. 1997 (100) No difference in physical
 performance between 2 trials (work
 done at the last 20 min maximal
 exercise), CWT improved after
 exercise-BCAA trial.
Mittleman et al. 1998 (106) Increased time to exhaustion with
 BCAA, increase in plasma BCAA and
 decrease tryptophan:BCAA. Trend to
 higher plasma ammonia. No
 difference between genders.
Blomstrand & Saltin, 2001 (107) BCAA have an anablic effect on
 muscle protein metabolism during
 recovery. Protein synthesis
 stimulated and/or protein
 degradation decreased as an effect
 of BCAA ingestion. However during
 exercise the data is too variable
 to make any conclusion.

(a)RDBPCX: randomised double-blind placebo control crossover, RPC:
randomised placebo control, DBPCX: double-blind placebo control,
crossover, PC: placebo control, PCX: placebo control crossover.

(b)CHO: carbohydrate, BCAA: branched chain amino acids, Val: valine,
Leu: leucine, Ile: isoleucine.

(c)[VO.sub.2max]: maximal Oxygen consumption during exercise, CWT:
Stroop Colour Word Test.

Table 4

Summary of research studies on carnitine supplementation in exercising,
trained or untrained individuals, from 1988-2000 (n = 11)

Study Subjects Study type (a)

Soop et al. 1988 (130) 7M (moderately CX (own controls)
 trained)

Vecchiet et al. 10M (moderately RDBPCX
1990 (124) trained)

Siliprandi et al. 10M (moderately RDBPCX
1990 (125) trained)


Decombaz et al. 9M (untrained) DBPCX
1993 (131)


Natali et al. 1993 (122) 12M (healthy active) RPCX


Arenas et al. 16M (well-trained long- RDBPC
1994 (126) distance runners)


Barnett et al. 8M (healthy males) EP-2 controls
1994 (132)

Brass et al. 1994 (123) 14M (healthy males) RDBPCX



Trappe et al. 20M (highly-trained RDBPC
1994 (129) swimmers)


Vukovich et al. SM (healthy males) R, C (1st trial) 3
1994 (133) trials

Colombani et al. 7M (endurance-trained RDBPCX
1996 (127) athletes)



Study Carnitine dose trial

Soop et al. 1988 (130) 5 g/d (orally)-5 days


Vecchiet et al. 2 g (orally) @ 1 h
1990 (124) before exercise (acute
 administration)
Siliprandi et al. 2 g (orally) @ 1 h
1990 (125) before exercise (acute
 administration)

Decombaz et al. 3 g/d (orally)-7 days
1993 (131)


Natali et al. 1993 (122) 3 g(intravenously)-1
 dose 40 min before

Arenas et al. 2 g/day (orally)-28
1994 (126) days


Barnett et al. 4 g/day (orally)-14
1994 (132) days

Brass et al. 1994 (123) 92.5 mol/kg or
 18.5 mol/kg
 (intravenously)
 administration-1 dose
Trappe et al. 4 g/day (orally)-7
1994 (129) days 2 g twice daily


Vukovich et al. 6 g/day (orally) 7-14
1994 (133) days

Colombani et al. 4 g (orally) 2 g @ 2 h
1996 (127) before run and 2 g @
 20 km mark


Study Event/Exercise test (b) Effect

Soop et al. 1988 (130) Cycling 120 min @ 50% [VO.sub.2max] No


Vecchiet et al. Cycling ergometer until exhaustion, Yes
1990 (124) 72 hours rest and repeated exercise
 test
Siliprandi et al. Cycle to exhaustion (2 bouts of Yes
1990 (125) maximal ergometer) separated by a
 3-day interval

Decombaz et al. Cycling 20 min at 60% [VO.sub.2max] No
1993 (131) + CHO depletion regime


Natali et al. 1993 (122) Cycling 40 min @60 w + 2 min No
 anaerobic exercise (250W) + 50 min
 for recovery
Arenas et al. Running 40-50% [VO.sub.2max] 90 Yes
1994 (126) min/d for 5 days and 70-80%
 [VO.sub.2max] 60 min/d for 2 days

Barnett et al. Sprint cycling 90% [VO.sub.2max]/4 No
1994 (132) min, rest 20 min and 5 x 1 min ride
 at 115% [VO.sub.2max]
Brass et al. 1994 (123) Bicycle ergometer test (RQ, FFA No
 glucose utilisation, [VO.sub.2] at
 fixed workload)

Trappe et al. Swimming bouts 5 x 91.4 m (100 yd) No
1994 (129) at supra-maximal intensity, 2 min
 rest each

Vukovich et al. Submaximal exercise (cycled 60 min No
1994 (133) at 70% [VO.sub.2max] - RQ, FFA
 glucose utilisation, [VO.sub.2])
Colombani et al. Marathon run + submaximal No
1996 (127) performance test day after marathon
 + post-race lactate


Study Comments

Soop et al. 1988 (130) No effect on muscle substrate
 utilisation during exercise and at
 rest.
Vecchiet et al. Increased time and work until
1990 (124) exhaustion, decrease in lactate
 production and oxygen uptake.
Siliprandi et al. Increased time to exhaustion.
1990 (125) Post-exercise increase in plasma
 lactate and pyruvate was after
 maximal progressive work.
Decombaz et al. No metabolic enhancement, substrate
1993 (131) metabolism not affected during
 submaximal exercise. Performance
 was not measured.
Natali et al. 1993 (122) No changes during exercise, but
 increased fatty acid oxidation
 during recovery.
Arenas et al. Improvement in [VO.sub.2max] based
1994 (126) on biochemical findings and
 significant increase in the
 pyruvate dehydrogenase.
Barnett et al. No significant effect on muscle
1994 (132) carnitine content and thus could
 not alter lactate accumulation.
Brass et al. 1994 (123) No effect on fuel metabolism during
 exercise in humans.


Trappe et al. No ergogenic benefit during
1994 (129) repeated bouts of high-intensity
 anaerobic exercise in highly
 trained swimmers.
Vukovich et al. No effect on lipid or carbohydrate
1994 (133) oxidation during exercise.

Colombani et al. No changes in exercise metabolism
1996 (127) or marathon running time, no change
 in recovery and submaximal test
 performance post race.

(a)RDBPC: randomised double-blind placebo control, RDBPCX: randomised
double-blind placebo control crossover, RPCX: randomised placebo control
crossover, CX: crossover, DBPCX: double-blind placebo control crossover,
RC: randomised and control, EP: experimental protocol.

(b)[VO.sub.2max]: maximal Oxygen consumption during exercise,
[VO.sub.2]: oxygen consumption, RQ: respiratory quotient, FFA: free
fatty acids.

Table 5

Summary of recent studies on supplementation with popular ergogenic aids
and physical performance


Supplement Evidence of Condition for an ergogenic effect
 type efficacy

 Creatine Clear evidence High-intensity, short-term exercise
 of efficacy tasks ([less than or equal to]30
 seconds, repeated exercise bouts
 and limited recovery time between
 repetitions.
 HMB (a) Evidence of Gains in strength and body mass
 efficacy is associated with resistance
 limited training, and recovery from exercis
 population. healthy population
Glutamine No ergogenic effect



 BCAA (b) No ergogenic effect

Carnitine No ergogenic effect


 N[degrees] of
Supplement Comments examined
 type trials

 Creatine No significant effect in aerobic 35
 endurance exercise tasks. Further
 research is needed (long-term
 studies, safety, side effects).

 HMB (a) Studies mainly positive for novice 8
 rather than well-trained athletes.
 Limited number of studies.

Glutamine Clinical evidence in the 8
 maintenance of muscle mass and
 immune system function in
 critically ill patients.
 BCAA (b) No ergogenic effect, further study 9
 is needed.
Carnitine Study design limitations, further 11
 research is needed.

(a)HMB: hydroxymethylbutyrate.

(b)BCAA: branched chain amino acids.


Acknowledgment

Acknowledgment is given to Dr Peter Williams who gave valuable assistance and helpful comments as a supervisor.

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This paper derives from a project that was completed in partial fulfillment of the MSc (Nutrition) course, in the Department of Biomedical Science at University of Wollongong, NSW G. Beduschi, MSc, BNutrDiet, Lecturer, FEPAR University, Parana, Brazil

Correspondence: G. Beduschi, R: Augusto Stellfeld, 1387, Bigorrilho, Curitiba -- Parana, Brazil 80430-140. Email: grazibedu@hotmail.com
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