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Endogenous CHO reserves are limited, and muscle and liver glycogen depletion often coincide with fatigue during both endurance events and many team sports. Consequently, it has been speculated that an increased availability of FA in the circulation (via the consumption of a high-fat diet or a fat-rich meal) should, in theory, ‘spare’ endogenous CHO stores, promote lipid utilisation and improve endur-ance performendur-ance in trained individuals. Several exercise–nutrition interventions have received scien-tific investigation and these are now discussed.

Fat feeding before exercise

Many studies have investigated the effects of acute fat feeding before aerobic exercise on the subsequent rates of substrate oxidation and exercise perfor-mance. The results from these investigations are equivocal with regard to the effect of fat feeding on muscle metabolism and also performance outcomes.

In early studies, fat feeding in combination with intravenous administration of heparin was shown to stimulate lipolysis, elevate plasma FA concentrations and decrease rates of muscle glycogen utilisation by as much as 40% compared with a control condition during 30 min of submaximal running. On the other hand, other investigations have reported only small differences in the rates of fat oxidation in response to high-fat meals ingested in the hours before pro-longed submaximal cycling. An interesting observa-tion from some of these reports is that most of the differences in substrate metabolism favouring fat oxidation (i.e. a lower RER) after fat feeding were only evident in the early stages of exercise, and did not result in an improved performance time.

Long- and medium-chain triglyceride ingestion during exercise

Thirty years ago the effects of ingestion of medium-chain fatty acids (MCFA) versus long-medium-chain fatty acids (LCFA) on FA oxidation during exercise were compared. The theoretical potential of MCFA as an energy source during exercise is based on the more efficient uptake and oxidation in skeletal muscle.

Lipids (∼30 g) were ingested by 10 well-trained subjects 1 hour before a bout of moderate-intensity exercise lasting 60 min. LCFA ingestion increased

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serum TG concentrations but neither MCFA nor LCFA had any effects on the rates of whole-body FA oxidation. When more than 50 g of MCFA or LCFA were ingested, severe gastrointestinal problems were experienced by the majority of subjects, and at the time it was recommended that a maximum amount of only 30 g of ingested FA could be tolerated by most individuals. Other studies have utilised stable isotope tracers ([1-¹³C] octanoate, [1-¹³C] palmitate) to track the fate of ingested MCFA and LCFA on rates of fat and CHO oxidation and exercise time to exhaustion during submaximal exercise. These experiments revealed that MCFA ingestion was associated with a rise in blood ketone bodies, which are potential energy sources. On the other hand, blood ketone con-centrations were unchanged with LCFA ingestion.

In contrast to LCFA, which slow the rate of gastric emptying and enter the systemic circulation as chylomicrons, MCFA are emptied very rapidly from the intestine to the liver and are quickly metabolised.

In the 1990s researchers compared the oxidation of ingested MCFA with glucose during 2 hours of cycling at 65% Vo_2max. It was found that the contribution of MCFA and glucose to total energy requirements during exercise was similar between the two interventions. The effects of a combination of CHO and MCFA ingested during 3 hours of moderate-intensity exercise (57%

Vo_2max) in well-trained cyclists have also been investi-gated. When 10 g of MCFA was co-ingested with CHO each hour, about 70% of the MCFA consumed was oxi-dised compared with only 33% when MCFA was ingested alone. Towards the end of exercise, the rate of ingested MCFA oxidation closely matched the rate of ingestion. Even so, the contribution of ingested MCFA to total energy expenditure was only 7%. Subsequent work revealed that MCFA ingestion had little effect on rates of muscle glycogen utilisation during 180 min of moderate-intensity cycling. Indeed, even when subjects commenced exercise with low muscle glycogen con-tent, MCFA ingestion had no effect on CHO utilisation and even though low glycogen resulted in increased fat oxidation, MCFA oxidation was not increased. Finally, a recent study compared the ingestion of CHO (60 g/

hour) with a CHO (60 g/hour) plus MCFA (∼24 g/

hour) solution on cycling time trial performance.

Subjects completed a set amount of work equal to about 100 km as fast as possible. Compared with a pla-cebo (178 ± 11 min), the time to complete the ride was reduced after the ingestion of both CHO (166 ± 7 min)

and CHO plus MCFA (169 ± 7 min). Thus, the addition of the MCFA did not provide any further performance enhancement over CHO alone.

To date, only one study has reported a beneficial effect of MCFA ingestion on FA metabolism and per-formance. In that investigation it was shown that when large doses (∼30 g/hour) of MCFA were co-ingested with a 10% glucose beverage, serum FA con-centrations were elevated, FA oxidation was increased, estimated muscle glycogen utilisation reduced, and 40-km cycle performance (which followed 2 hours of submaximal exercise at 60% Vo_2max) improved by 2.5% compared with when glucose was ingested alone. However, it should be noted that the results from this investigation are the exception. Indeed, as noted earlier, the ingestion of large amounts of MCFA (>15 g/hour) are likely to produce gastrointestinal problems in most athletes, which would be expected to be detrimental to performance. In a recent study the effect of specific structured TGs on performance was evaluated. In contrast to MCFA, which consists of three medium-chain fatty acids, the specific struc-tured TGs combined medium-chain and long-chain FAs (MLM). This combination of fatty acid chain length has been shown to avoid gastrointestinal distress and might improve performance. Specific structured TG (MLM) together with CHO or CHO alone was administered to well-trained subjects dur-ing 3 hours’ cycldur-ing at 55% Vo_2max followed by a time trial (∼50 min duration). Exercise performance was similar in both trials. Taken collectively, the results of the studies reviewed here clearly demonstrate that there is no beneficial effect of ingestion of MCFA or specific structured TG (MLM) on endurance perfor-mance and/or exercise capacity. The lack of an effect on performance may seem surprising, but only one study actually measured the concentration of MCFA (8:0 FAs) in plasma and in that experiment it was not possible to detect 8:0 FA. The lack of an increase in plasma FA concentrations, specifically 8:0 FA, may partly explain why muscle metabolism and perfor-mance outcomes are not different.

Consumption of high-fat low-carbohydrate diets

It has long been known that modifying an individu-al’s habitual diet can significantly alter the subse-quent patterns of substrate utilisation during aerobic

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exercise and impact on subsequent exercise capacity and/or performance. The consumption of a high-fat (>60% of energy intake) low-CHO (<15% of energy) diet for 1–3 days markedly reduces resting muscle glycogen content and increases FA oxidation during submaximal exercise. Such a shift in substrate utilisa-tion is commonly associated with impairment in exercise capacity In contrast to the negative effects on exercise capacity that seem to result from short-term (1–3 days) exposure to high-fat diets, there is some evidence to suggest that longer periods (5–7 days) of adaptation to high-fat diets may induce adaptive responses that are fundamentally different to the acute lowering of body CHO reserves. It has been proposed that such adaptations eventually induce a reversal of some of the mitochondrial adaptations that favour CHO oxidation and ‘retool’ the working muscle to increase its capacity for FA oxidation.

A frequently cited study to support the use of high-fat diets to improve athletic performance was conducted in the mid-1980s. In this investigation the effects of 28 days of a high-fat diet (85% of energy) versus a eucaloric diet containing 66% of energy from CHO on submaximal cycle time to exhaustion was tested. The high-fat diet reduced the average rest-ing muscle glycogen content of the five trained study subjects by 47%; consequently, when cycling at approximately 63% Vo_2max, RER values were 0.72 (95% of energy from fat, 5% from CHO) and 0.83 (56% of energy from fat, 44% from CHO) for the high-fat and normal diets, respectively. Remarkably, the mean exercise time at this moderate work inten-sity was not statistically significantly different after the two dietary interventions (147 vs. 151 min for the eucaloric vs high-fat diets, respectively).

In the mid-1990s a South African laboratory used a random cross-over design to investigate the effects of 14 days of either a high-fat (67% energy) or a high-CHO (74% energy) diet in five trained cyclists.

After dietary adaptation, subjects undertook a com-prehensive battery of physical tests including a 30-s Wingate anaerobic test, a ride to exhaustion at about 90% Vo_2max and, following a 30-min rest, a further ride to volitional fatigue at 60% Vo_2max. Although the high-fat diet significantly reduced pre-exercise mus-cle glycogen content by almost 40% (from 121 mmol/

kg w.w. after the normal diet to 68 mmol/kg w.w. after the high-CHO diet), mean 30-s anaerobic power was similar between the two conditions (862 vs. 804 W

for the high-fat and high-CHO diet, respectively).

Neither was there an effect of dietary manipulation on the time subjects could ride at a work rate eliciting about 90% Vo_2max (8.3 vs. 12.5 min for the high-fat and high-CHO trials). Indeed, the only effect of the high-fat diet was to prolong submaximal endur-ance time during the third and final laboratory test (ride to exhaustion at 60% Vo_2max) from 42 to 80 min, despite significantly lower starting muscle glycogen content (32 vs. 73 mmol/kg w.w.). Such increases in endurance were associated with a marked decrease in the average rate of CHO oxidation (2.2 vs. 1.4 g/min) and a significant increase in the rate of fat oxidation (from 0.3 to 0.6 g/min). The results of this investiga-tion are difficult to interpret because of the unortho-dox study design, but they strongly suggest that submaximal exercise capacity can be preserved despite low pre-exercise muscle glycogen content when trained individuals are adapted to a high-fat diet.

Probably the longest exposure to a CHO-restricted diet was performed by a Danish group who exam-ined diet–training interactions in two groups of 10 untrained subjects participating in a 7-week endur-ance training programme while consuming either a high-fat (62% energy) or high-CHO (65% energy) diet. Cycle time to exhaustion at 70% Vo_2max increased by 191% after the high-CHO diet, but only by 68% in those subjects who consumed the high-fat diet. These findings clearly demonstrate that a combination of training and a fat-rich diet do not reveal an additive effect on physical performance. In summary, com-pared with a high-CHO diet, a period of adaptation to a high-fat diet increases the relative contribution of FA oxidation to the total energy requirements of exercise by up to 40%. However, adaptation to a high-fat diet does not appear to alter the rate of muscle glycogen utilisation or improve prolonged moderate-intensity exercise. Adaptation to a high-fat diet is only likely to impact on endurance perfor-mance in sporting situations where CHO availability is limiting. More to the point, such nutritional strate-gies are only likely to be of benefit to a small group of highly trained endurance or ultra-endurance ath-letes. Although it has been suggested that as long as 20 weeks of exposure should be allowed if humans wish to adapt to high-fat diets, such a time-frame is both impractical and could pose health problems for athletes. Exposure to high-fat diets is also associated with insulin resistance in the liver, resulting in failure

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to suppress hepatic glucose output, and an attenua-tion of liver glycogen synthesis. For these reasons, caution should always be exercised when sports prac-titioners recommend high-fat diets to athletes.

Short-term ‘adaptation’ to high-fat diets followed by acute

high-carbohydrate diets

Over 20 years ago it was proposed that nutritional preparation for endurance and ultra-endurance events should encompass periods of ‘nutritional periodisation’. In such a scenario athletes might train for most of the year on a high-CHO diet, adapting to a high-fat diet for several days early in the week prior to a major event, then CHO loading in the final 48 hours immediately prior to competi-tion. Such nutritional periodisation would still permit endurance athletes to train hard throughout the year and maximise their endogenous CHO stores before competition, while theoretically allowing the working muscles to optimise their capacity for FA oxidation during a major endurance race. More to the point, a short (3–5 days) period of exposure to a high-fat diet represents a practical period for extreme dietary change while minimising any poten-tial health risks. Indeed, it appears that most of the adaptive responses that facilitate an increased rate of FA oxidation are complete after as little as 5 days on a high-fat diet, and therefore nutritional periodisa-tion would seem a prudent and perhaps optimal strategy for endurance and ultra-endurance athletes to follow.

A series of investigations designed to determine the effects of either 5 days’ adaptation to a high-fat diet (fat 4.0 g/kg/day, CHO 2.4 g/kg/day) followed by 1 day of CHO restoration, or an isoenergetic CHO (9.6 g/kg/day) diet on metabolism and/or endurance and ultra-endurance cycling performance have been undertaken by a group of Australian researchers.

Competitive cyclists or triathletes with a history of regular endurance training were recruited for these studies: such individuals have the muscle adaptations which favour FA oxidation. During the initial investi-gation, muscle biopsies and tracer-derived estimates of blood glucose oxidation were determined. During a second study, subjects were given a pre-trial break-fast similar in size and composition to that which they might consume before a race. In addition, they

were allowed to consume CHO throughout the ride.

Such nutritional practices are currently recom-mended by sports nutritionists. Both investigations employed the same dietary intervention protocol before the laboratory exercise regimen (i.e. 5-day adaptation to a high-fat or high-CHO diet followed by 1 day of CHO restoration).

In agreement with the results from earlier studies, 5 days of a high-fat diet drastically reduced resting muscle glycogen concentration. However, 1 day of a high-CHO diet was sufficient to restore muscle gly-cogen concentration to normal resting levels. During 2 hours of cycling at 70% Vo_2max, muscle glycogen utilisation was less after fat adaptation (554 to 294 mmol/kg d.m.) than after the high-CHO diet (608 to 248 mmol/kg d.m.). This glycogen ‘sparing’

(100 mmol/kg d.m.) occurred because the rates of FA oxidation were elevated by about 50% above the CHO trial. Yet despite such substantial glycogen sparing, the performance of a time trial undertaken after 2 hours of submaximal cycling was similar between dietary treatments.

Unfortunately, the techniques utilised in these studies did not enable the determination of whether the elevated rates of FA oxidation were due to an increase in FA release, uptake and oxidation, or an increased reliance on TG. However, despite the brev-ity of the adaptation period, the high-fat diet elicited large shifts in favour of FA oxidation during submax-imal exercise. Such an adaptation is impressive in light of the already enhanced capacity for FA oxida-tion in such highly trained subjects. Because the con-ditions of the first trial (i.e. an overnight fast, water ingestion throughout exercise) are not commensu-rate with the nutritional practices of athletes, in a follow-up investigation subjects consumed a pre-trial breakfast and ingested CHO throughout the ride. As CHO ingestion effectively eliminates any rise in plasma FA concentration, an effect that can persist for several hours after ingestion, it would be expected that FA oxidation would also be suppressed during exercise. Compared with the first experiment, the overall rate of FA oxidation was lower. However, total FA oxidation was still higher after the high-fat diet compared with the high-CHO diet, indicating that there are persistent metabolic adaptations to a high-fat diet even when CHO availability during exercise is high. Although time trial performance was similar after the two dietary regimens, the results of this

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study provide strong evidence that the muscle can be

‘retooled’ to enhance FA oxidation in as little as 5 days, even when CHO is ingested before and throughout exercise. As such, this nutritional periodisation may still confer a positive benefit to those athletes involved in ultra-endurance sports lasting longer than 5 hours, when the need to conserve glycogen as long as possi-ble is of utmost importance for performance.

In an effort to identify some of the mechanisms in skeletal muscle that might be responsible for these shifts in fuel oxidation, muscle pyruvate dehydroge-nase (PDH) and hormone-sensitive lipase (HSL) activities were measured in biopsy samples taken before and after 20 min of cycling at 70% Vo_2max in subjects who followed the same fat-adaptation, CHO-restoration protocol. Confirming the previous results, resting muscle glycogen levels were similar after both dietary regimens, but RER values were lower during submaximal cycling after fat adapta-tion, which resulted in roughly a 45% increase and a 30% decrease in fat and CHO oxidation, respectively.

PDH activity was lower at rest and throughout exer-cise at 70% Vo_2max (1.69 ± 0.25 vs. 2.39 ± 0.19 mmol/

kg w.w./min). Estimates of muscle glycogenolysis during the first minute of exercise at 70% Vo_2max were also lower following fat adaptation. HSL activity tended to be higher during exercise at 70% Vo_2max following fat adaptation. These results indicate that the previously reported decreases in whole-body CHO oxidation and increases in fat oxidation follow-ing the fat-adaptation protocol are a function of metabolic changes within skeletal muscle. Moreover, the glycogen sparing observed in previous studies may actually be an impairment of the rate of muscle glycogenolysis, an adaptation that would not be ben-eficial for performance of high-intensity exercise. In support of this hypothesis, a recent study has reported that fat adaptation increased rates of fat oxidation during a 100-km time trial. However, repeated 1-km sprints (to mimic race conditions) performed at regular intervals during the 100-km ride were com-promised by fat adaptation compared with an isoen-ergetic high-CHO diet.

The possibility exists that 1 day of CHO intake after fat adaptation might not be sufficient duration to impact on endurance performance. In another investigation, the effects of 7 days of a high-CHO diet following 7 weeks of adaptation to a fat-rich diet (62% energy) versus an isoenergetic CHO diet (65%

energy) for 8 weeks (control trail) on endurance cycling performance were determined. Pre-exercise muscle glycogen stores were significantly higher (872

± 59 mmol/kg d.w.) after 7 days of CHO restoration compared with the control trial (688 ± 43 mmol/kg d.w.). Yet despite the higher muscle glycogen content, the impairment in endurance performance observed after the high-fat diet could not be reversed when subjects switched to the high-CHO diet during the eighth week. Even after a week of ingestion of CHO, the mean performance time was still approximately threefold lower than when the CHO-rich diet was consumed during the 8-week period. The authors concluded that ‘fat adaptation impaired the utilisa-tion of carbohydrates rather than spared carbohy-drate as an energy source during exercise.’

6.4 Summary

Many nutritional–exercise manipulations have been

Many nutritional–exercise manipulations have been