Several recent reviews have described in detail the effects of exercise on fat metabolism as well as the effects of various methods to modify fat metabolism in the athlete (220-222). The most important aspects are outlined below.
As pointed out earlier there is a progressive shift to the use of CHO oxidation with increasing exercise intensity. This has its origin in stronger metabolic and hormonal responses which induce an enhanced glycogen breakdown and lactate formation, as well as progressively increased recruitment of fast twitch muscle fibres, which generally lack the capacity to oxidize substantial amounts of FA.
Since the storage of CHO in the form of glycogen is limited, the ability to perform high intensity exercise will be decreased with progressive glycogen depletion (332). Any adaptation leading to an increased capacity to use FA for ATP resynthesis will lead to a sparing of endogenous CHO with the consequence that endurance capacity may be improved. Theoretically there may be a number of intervention possibilities to increase plasma FA levels and to improve the mechanisms involved in transport and oxidation of FA. Most of these interventions have been studied over the last three decades:
Endurance training has been observed to result in a number of structural and metabolic adaptations, which will favour FA oxidation. Whereas a-adrenergic mechanisms regulate lipolysis at rest, ^-adrenergic activity has been found to determine lipolysis during exercise (430). The sensitivity of fl-
adrenoceptors for catecholamines in the adipocyte will increase as a result of exercise (467). Sensitivity may be further enhanced as a result of adaptation to regular training. In addition, training will help fat cells to increase their sensitivity to stimuli for FFA mobilization, thereby improving the speed of adaptation to the higher needs when exercising (19). During maximal exercise intensity, however, the hormonal and metabolic stimuli to enhance CHO mobilization and along with it the mobilization, uptake and utilization of FAs, are maximized. In this condition the resulting increase in blood FFAs does not automatically lead to a reduction of muscle and liver glycogen utilization (7,162). This will theoretically promote the delivery of FA from the fat cells to the blood. However, recently it was shown by Romijn et al. (461) that the rate of appearance of FA from adipose tissue is decreased in the trained individual.
The capillary density of muscle tissue will increase, which in itself augments the exchange surface area, promotes blood flow and with it the delivery of oxygen and FA (437, 438). Training also induces an increase in sarcolemmal fatty acid binding protein, which contributes to the translocation of FA into muscle (452). Within the muscle cell there will be an increased mitochondrial volume as well as mitochondrial enzyme activity (463).
Trained muscles express a higher activity of LPL, muscle lipase, fatty acyl CoA synthetase and dehydrogenase, carnitine-acyl transferase and 3-hydroxyacyl CoA dehydrogenase, which will be in favour of enhancing FA supply to the mitochondria and subsequent oxidation (463). As a result, trained muscles are able to oxidize more substrate (438), which is also expressed in increased oxygen consumption at maximal exercise intensities (436, 457).
Lastly, trained muscles store more intracellular fat in lipid droplets located along the surface of the mitochondrial system; they may theoretically enhance the capacity to supply and oxidize FA derived from the intracellular lipid store (463).
Increased intracellular TG storage as well as observations from arteriovenous difference and isotope labelling experiments indicate that highly trained endurance athletes rely more on the utilization of intramuscular stored FA during exercise and less on the utilization of blood-borne FA (220, 463). The advantage of a shift from extracellular to intracellular stores of FA is that some potential barriers in overall FA utilization, such as the endothelium and the sarcolemma, are irrelevant when intracellular TG is utilized.
Thus, training enhances total FA oxidation, especially by increasing intramuscular fat storage and maximal FA flux. Along with this, endogenous CHO stores will be conserved during exercise in the endurance trained individual, which prolongs the time period during which intense exercise can be performed.
MEDIUM CHAIN TRIACYLGLYCEROL (MCT) INGESTION
MCT contains fatty acids with a chain length of six, eight or ten carbon atoms. Generally, MCT is rapidly emptied from the stomach and taken up by the intestine (471). After absorption by the enterocyte MCT is transported with blood to the liver, in contrast to long chain triacylglycerol (LCT) which is transported by the lymphatic system to the vena cava. MCT readily increases plasma medium chain FA and TG levels. In muscle, medium chain FA is rapidly taken up by the mitochondria, not requiring the carnitine transport system (22). Consequently, MCT is oxidized readily (7, 48, 111) and faster than LCT (435). This has led to the assumption that MCT may be an effective exogenous fuel for exercising muscle and that MCT ingestion may potentially enhance fat oxidation and thereby reduce CHO utilization.
Early studies have indicated that oral MCT, taken shortly before exercise, is only partly oxidized during exercise and has not been shown to improve performance (7, 92 162). In a study by Ivy et al. (92) 30-60 g of MCT were ingested with a cereal meal 1 h prior to exercise. Most probably because of the relatively low oxidation of the oral MCT, no differences in CHO oxidation were found. In two other studies there was a substantial oxidation of the ingested MCT (48,111,455). However, in these studies the amounts of MCT ingested were relatively small. Unfortunately, the effect of MCT feedings on performance was not measured in any of these studies.
More recently several stable isotope studies have been performed to evaluate the effect of MCT or MCT + CHO ingestion on exogenous, endogenous and total fat and CHO oxidation. These studies have shown that oral MCT is rapidly oxidized by muscle but does not lead to glycogen sparing in active muscle cells as measured from muscle biopsy specimen (446-449). The fact that total fat oxidation remained the same after MCT ingestion, even in a glycogen depleted state (446), points to the fact that oral MCT most likely competes with long chain FA and, hence, leads to a sparing of endogenous fat stores, probably intramuscular fat. This may also explain why no endogenous CHO sparing took place. Also in the studies of Jeukendrup et al. (446-449) relatively small amounts of MCT were supplied to the athletes. The background of this small supply was that ingestion of >30 g in a short period of time induces nausea and gastrointestinal discomfort. It may be speculated that this may be caused by a relatively high cholecystokinine (CCK) release after MCT intake (432).
In a recent study by van Zyl et al. (464), however, subjects ingested 86 g of MCT during submaximal endurance exercise lasting 2 h, followed by a 40 km time trial. Ingestion took place as 4.3% w/v MCT drink, 10% w/v CHO + 4.3% w/v MCT drink or 10% w/v CHO drink as control. Interestingly, they observed the poorest performance with ingestion of MCT alone but a significantly improved performance with the CHO + MCT
trial compared to the CHO trial. No mention was made of any gastrointestinal discomfort. The authors did not measure muscle glycogen but speculated on the basis of a reduced endogenous CHO oxidation that glycogen may have been spared and that this might explain the performance benefit observed. These findings are in contrast to the earlier mentioned observations by Jeukendrup et al. (446) who observed no endogenous CHO or glycogen sparing. This has prompted Jeukendrup et al. (449) to perform a similar experiment in which the subjects ingested 85 g MCT as MCT drink, CHO + MCT drink or for control a placebo drink during an endurance exercise lasting 2 h at an intensity of 60% VO2max, followed by a 15 min time trial. In this particular study the performance test was not interfered with by any physiological measurement. In contrast to the study of van Zyl et al. (464), performance was not improved by the MCT + CHO treatments. A substantial number of subjects experienced gastrointestinal problems with MCT ingestion. The reason for the discrepancy in the data of these studies remains unclear.
Thus, from the available data it cannot be concluded that MCT ingestion is of benefit for glycogen sparing and/or improving endurance performance.
Another attempt to improve fat oxidation has been to enhance the blood long chain FA levels by infusing lipid emulsions. This procedure has been shown to result in a significant reduction of glycogen degradation in two studies (445, 466). In line with the positive effects of fat infusion on muscle glycogen sparing, the opposite—a decline of plasma FA, induced by inhibiting lipolysis by nicotinic acid—resulted in an increased rate of muscle glycogen degradation (431). An elevated level of circulating FA is thus a prerequisite for reducing the rate of endogenous CHO utilization during exercise. However, for sports practice this procedure seems to be impractical. Infusions during competition are not possible and even if they were, the IOC doping regulations, which consider any artificial measure to enhance performance as unethical, would forbid them.
Oral intake of fat emulsions may not be of benefit either. Oral fat may inhibit the gastric emptying rate of rehydration solutions also ingested during exercise and may lead to gastrointestinal discomfort (30). Additionally, it will take a considerable time before the absorbed long chain triacylglycerols will be available for oxidation because of passage through the lymphatic system.
To our knowledge there are currently no studies that have convincingly shown any benefit of fat ingestion shortly before or during exercise. One study (490) pointed to a favourable effect of ingesting a high fat meal 3 hours before exercise, in combination with a heparin infusion (improving fatty acid mobilisation). The latter, however, would fall under the doping regulations. A study with a high fat meal alone (406) showed no effect. Thus, although oral supply of fat may increase the blood fat level, the uptake of fat from blood into active muscle cells may not be enhanced due to limitations in the FA transport capacity (19, 220, 463). In this respect, fat supply during exercise in trained subjects during competition conditions has not been shown to be of benefit for a reduction of muscle and liver glycogen utilization (7, 162).
Caffeine is known to affect muscle, adipose and central nervous tissue indirectly by mediating the level of cyclic adenosine monophosphate (cAMP) and its related calcium release from the intracellular storage sites (220). This effect is initiated by binding of catecholamines to beta-receptors of cell membranes, thereby enhancing the activity of the enzyme adenylate cyclase, which catalyses the formation of cAMP from ATP. Caffeine has been observed to enhance plasma norepinephrine and epinephrine levels. Additionally, caffeine inhibits phosphodiesterase which degrades cAMP to the non-active compound 3 '5 '-AMP. In this way caffeine increases cAMP half-life and with it lipolysis. By these actions caffeine increases the cAMP level which maximizes the activity of the intra-adipocyte lipase and, hence, lipolysis.
Nevertheless, caffeine has been observed to enhance plasma FA in many studies in man and animals (220, 327, 332). In contrast, an increased fat oxidation (by assessment of the respiratory exchange ratio, RER) and reduced glycogen degradation were observed in only a few of these studies. This may indicate that the caffeine-induced elevation of FA simply comes on top of the relatively high exercise-induced increase in FA, which most likely already maximizes FA transport across the epithelium. These data also indicate that the performance-enhancing effects of caffeine (see also pages 149-159) are most probably related to effects on the central nervous system rather than to effects on fat oxidation and glycogen sparing.
There are reasons to hypothesize that caffeine ingestion may indirectly also counteract its effect on lipolysis and subsequent FA oxidation during exercise. Increased liver glycogen breakdown and plasma lactate levels have been observed after caffeine ingestion (220) and lactate is known to be a strong inhibitor of lipolysis (439). Thus it cannot be excluded that caffeine might also exert depressing effects on FA oxidation in exercising muscle cells.
In humans carnitine is obtained from the diet, especially from red meat. Additionally, carnitine is synthesized in the body from intracellular trimethyllysine, which requires methionine for the methylation process. This biosynthetic process occurs mainly in liver and to a smaller extent in kidney and brain (442) after which l-carnitine is released into the circulation from which it is taken up by muscle. l-Carnitine is lost daily in small amounts from the body via urine and stools. The primary function of l-carnitine is the transfer of long chain FA across the mitochondrial membrane (434), to enter the oxidation pathway.
Addition of l-carnitine to the incubation medium has been shown to markedly enhance the long chain FA oxidation of isolated mitochondria (434). This has led to the speculative assumption that oral l-carnitine intake should lead to enhanced fat oxidation in athletes or in people wanting to lose weight. However, there is no solid scientific evidence that this is the case, despite the enormous amount of positive performance claims made in advertisements for this nutritional aid, as under normal conditions tissue carnitine levels are relatively high and do not form a constraint on FA oxidation.
Oral l-carnitine has been observed to increase the plasma l-carnitine level while uptake in muscle remained unchanged (462). This observation fits well with the finding that l-carnitine is taken up against a concentration gradient—plasma 40-60 mmol and muscle 3-4 mmol (433). This gradient is so large that even a substantial oral intake would not result in a measurable change in this situation. As a result of increased plasma levels and unchanged muscular uptake, urinary carnitine excretion increases many-fold (190).
Additionally, there are no indications that heavy exercise results in a substantial loss of carnitine from muscle cells. No differences in resting carnitine levels have been observed between training and non-training individuals (472). These data, as well as those of other well-controlled recent studies (473 -475), failed to show an effect of l-carnitine supplementation on FA oxidation of muscle during exercise (also see pages 145-146). For complete review see Wagenmakers (190, 264) and Heinonen (478).
High fat diets are claimed to enhance the capacity to oxidize FA and have attained considerable interest as a potential tool to improve performance in endurance athletes. In rats a high fat diet has been observed to increase LPL activity significantly, compared to animals fed a high CHO diet (460). However, this observation has to be interpreted with caution and may be explained by a strong upregulation of LPL activity with the used combination of high fat - low CHO in one group and a downregulation in the other group, receiving high CHO - low fat. Thus, most likely, such a striking difference may not appear when a high fat diet is compared to a normal mixed diet.
An increased LPL activity as well as an increased deposition of intracellular fat in muscle may explain a greater availability of FA to the mitochondria after a high fat diet and also may explain the lower RER (220). In rats a high fat diet also induced an improved performance (456). However, there may be significant species differences in FA handling. As such, human studies are of critical importance in order to draw any conclusions.
Johannessen et al. (450) studied seven male subjects who ingested a high fat diet in either solid or liquid form (76 en% fat) during 4 days, or a high CHO diet (76 en% CHO). This diet regimen was followed by a run endurance test till exhaustion. The running test consisted of alternating blocks of 30 min running followed by 10 min rest. Performance was significantly reduced (by approximately 40%) after this short-term high fat diet. Jansson and Kaijser (444) investigated the effect of a high fat diet lasting 5 days (69 en% fat) followed by a 5 day high CHO diet (75 en% CHO) on muscle substrate utilization in 20 subjects. FA utilization was estimated by measuring arteriovenous differences and by measurement of substrate concentrations in muscle biopsy specimens. Although they observed a lower RER after the fat diet and an increased FA extraction by muscle, there was no consistent effect on muscle glycogen utilization. The study included both males and females, was not randomized in treatment order and the diet duration was very short. No performance measures were taken. Phinney et al. (459) studied five cyclists who had to perform an endurance capacity test till exhaustion after a high fat diet lasting 4 weeks. The authors claimed that high fat diet caused a significant improvement in performance. However, the individual performance data show that only two out of five cyclists improved their performance, one of these two by 57%! Two showed a decreased performance and one cyclist remained on the same level. That the overall result was positive was largely on account of the single subject who showed the rather unrealistic 57% performance increase after one month on a high fat diet. Furthermore, no crossover design was used in this study. Lambert et al. (453) studied five well trained cyclists for a period of 14 days who ingested either a high fat diet (67 en% fat) or a high CHO diet (74 en% CHO). The high fat diet led to a reduction of muscle glycogen content of approximately 50% (121 ± 4 and 68 ± 4 mmol/kg w/w for high CHO and high fat treatment respectively). In a high intensity cycling test to exhaustion (85% VO2max) there were no statistically significant differences between the treatments, although the mean values were quite different in terms of athletic performance times (8.3 ± 2.3 and 12.5 ± 3.8 min for high fat and high CHO diet respectively). During a low intensity performance trial, which followed the high intensity trial after a rest period of 20 min, time to exhaustion was significantly prolonged. However, despite the fact that exhaustion occurred, the heart rate observed was only 142 ± 7 beats/min in the high fat diet and 143 ± 8
beats/min in the high CHO trial, in contrast to a heart rate of >180 beats/min in the high intensity trial. The fact that the preload (the high intensity test) was not standardized and that heart rate response does not reflect the stress of exercise-induced exhaustion points to the possibility that variables other than the difference in the diet alone, e.g. motivational, may have influenced the performance results. The very large difference in time to exhaustion in the low intensity (50% peak power output) trial (79.7 ± 7.6 min vs. 42.5 ± 6.8 min for high fat and high CHO diet respectively) further underlines this suggestion. It can be questioned whether such a large performance difference can be caused by 14 days of a high fat diet alone.
Muoio et al. (458) tested runners on a treadmill after a diet intervention lasting 3 weeks and observed a significant increase in time to exhaustion from 76 to 91 min while running at an intensity of 75-85% VO2max. Moreover, the 'high fat diet' consisted of 50 en% CHO and 38 en% fat. As such, this is comparable to a normal mixed diet consumed by many athletes. Thus, since there was no real high fat diet and no change in fat oxidation was observed, it is unclear whether this performance capacity improvement is the result of fat in the diet.
Hoppeler et al (485) compared the effect of a low fat diet (18.4%) to a high fat diet (40.6%) on endurance capacity during a run at 80% VO2max until exhaustion. VO2max remained unchanged but endurance capacity improved by 21%. It remains to be established whether such an effect also improves the performance to run a certain distance faster.
Helge and Kiens (441) studied the effect of combined training and diet on performance progression in 20 untrained subjects, divided into two groups of 10. These subjects performed endurance training for a period of 7 weeks, three or four times per week, while ingesting either a 65 en% CHO or a 62 en% fat diet. This period was followed by another training period of 1 week, while ingesting the CHO rich diet alone. The results showed that maximum oxygen consumption increased by 11% in both diet groups. Performance progression, however, was significantly better with the high CHO diet. From 35.2 ± 4.5 min to 102.4 ± 5.0 min in the high CHO diet and from 35.7 ± 3.8 min to 65.2 ± 7.2 min in the high fat diet, respectively. After the final week on the CHO diet, the performance improvement in the previous CHO-treated groups was maintained while the previous fat diet group further improved endurance performance from 65.2 ± 7.2 min to 76.7 ± 8.7 min. This, however, was still below the achieved performance of the CHO diet group; i.e. 103.6 ± 7.2 min. Heart rate and noradrenaline levels were highest while being on the high fat diet.
These results indicate that a high fat diet is detrimental with respect to training and performance progression at the beginning of an endurance training programme. This was the case despite the observation that the high fat diet resulted in a 25% increase in ^-hydroxyacyl-CoA-dehydrogenase, one of the key enzymes in FA oxidation, in the high fat diet group compared to no change in the CHO diet group. It should be emphasized, however, that these data do not allow for a generalization towards highly trained individuals.
To the best of our knowledge no other human studies on the effect of high fat diets are available at this moment. Seen against the bulk of the evidence that CHO ingestion improves endurance performance tasks, it remains speculative to state that a high fat diet, which downregulates CHO metabolism as well as may decrease glycogen stores in muscle and liver, may lead to better results. The fact that high fat diets are unpalatable restricts most attempts to study their effects in humans to a duration of several weeks at maximum. On the one hand this may be too short to achieve measurable adaptation effects. On the other hand, long-lasting trials may result in adverse health effects on the cardiovascular system as well as lead to insulin insensitivity, especially in less well trained subjects, due to overexposure of lipids to the body. Interestingly, in the available human fat diet performance studies, no systematic measurement of changes in lipoproteins were undertaken. Recently, Leddy et al. (454) reported data on 12 male and 13 female runners who, divided in subgroups, raised daily fat intake from 16 to either 30 or 40 en%, for 4 weeks. This increase in fat was not associated with changes in LDL cholesterol, apolipoprotein B or Apo A1 /Apo B ratio, but raised HDL cholesterol. This study indicates that shifting from a high CHO diet to a diet that has a fat content comparable to that of many sedentary individuals, is not associated with negative side effects for well trained athletes. Since most high fat diets tested and sometimes recommended to athletes have a substantially higher fat content, i.e. 50-65 en%, additional studies are required to evaluate the possible effects on cardiovascular risk factors.
The recent findings by Van Zyl et al. (465) point to the fact that a combination of a short-term high fat diet followed by a high CHO diet may improve endurance performance. They studied five trained cyclists who ingested in random order either their habitual diet or a high fat diet (65 en%) for 10 days, followed by a 3 day high CHO diet (65 en%). This dietary preparation was followed by an exercise preload of 2.5 h at an intensity of 70% VO2max, after which a 20 km time trial was performed. During the time trial the subjects ingested a CHO-MCT suspension. Time trial performance was improved by 80 s (p < 0.05) after the 7-day high fat and 3-day high CHO preparation. However, more studies and with a greater number of subjects need to be done before any well founded recommendations on this type of nutritional preparation can be made. No performance effects were observed by Burke (484) in 8 trained cyclists after a 5 day high-fat diet. Interesting in this regard are the observations made by Helge et al. (440) that a high fat diet lasting 7 weeks, irrespective of training, increases ^-hydroxyacyl-CoA-dehydrogenase activity in muscle
and that this effect does not occur in subjects following the same training programme but ingesting a CHO rich diet. This suggests that diet per se can influence endurance exercise-induced adaptations in muscle. Thus, from the paragraphs above it appears that although a number of intervention possibilities to enhance FA oxidation during exercise—with the goal to improve endurance capacity—have been studied, only regular endurance training can be classified as being successful in this respect. Although some very recent data after following a combined dietary intervention (CHO rich diet 2 short-term high fat diet 2 high CHO diet 2 competition) show improvements in performance during low intensity exercise, the bulk of evidence points to the fact that high intensity exercise performance is best achieved after being on a diet which is relatively high in CHO and low in fat. One other aspect should be mentioned. A substantial number of animal studies has shown that high fat diets result in insulin resistance and type II diabetic responses (43). The safety healthyness of a high fat diet for athletes has not been established in this respect.
Statements that l-carnitine, caffeine, MCT feedings, oral TG feedings and high fat diets may improve endurance performance of endurance athletes during high intensity events can at present not be supported by consistent and solid scientific evidence.
Sedentary people living in industrialized countries consume diets that contain 35-45% of total energy content as fat (19, 131). These figures are relatively high, seen in the light of recommendations that daily food should be rich in CHO (>50 en%). Athletes are generally advised to reduce fat intake to approximately 25-35 en%, thereby enhancing CHO intake to 55-65 en% (19, 39, 44, 45, 90,173). This reduced fat intake should to a large extent be realized by consumption of lean meat and low fat foods. Saturated fatty acid intake should be limited to less than 10 en%, mainly by making use of plant oils for meal preparation instead of hard saturated fats. With improved food quality and increased total energy consumption, the low figure of 25-35 en% fat intake in athletes will lead to a more than sufficient supply of the essential fatty acids that are required for normal biological functions (at least >1 en%, preferably about 7 en% should be in the form of mono- and polyunsaturated fatty acids (131)). Polyunsaturated fatty acids are known to influence the structure of the cell membrane especially of red blood cells. A group of French scientists (77) reported that an increased intake of omega-3 fatty acids, by means of supplementation (e.g. fish oil capsules), resulted in improved red blood cell plasticity, maximal oxygen consumption and better blood oxygen levels when exercising at high altitude. However, similar findings have never been reported when exercising at sea level. A recent study (223) performed at sea level did not result in any performance benefit. In this study fish oil rich in omega-3 fatty acids was given for a period of 3 weeks at 6 g daily. A significant increase in the amount of polyunsaturated fatty acids in the cell membranes of red blood cells was observed but the deformability of the red blood cells during exercise remained unchanged.
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