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Effects of short-term fat adaptation on metabolism and performance of prolonged exercise


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Medicine & Science in Sports & Exercise: September 2002 - Volume 34 - Issue 9 - p 1492-1498
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Endogenous carbohydrate (CHO) stores are limited and only sufficient to fuel ∼3 h of continuous, submaximal (70–80% maximal oxygen uptake [V̇O2max]) exercise: depletion of CHO reserves is associated with fatigue and impairment of exercise capacity (12). Typically, nutritional strategies aimed at optimizing performance of endurance (<3–4 h) or ultra-endurance (>5 h) sports have focused on techniques to increase CHO availability (1). Nutritional strategies such as CHO-loading (17), consuming a CHO-rich meal in the hours before exercise (15), and consuming CHO throughout an event (7) have been shown to enhance endurance performance when CHO availability is maintained or increased during the latter stages of prolonged exercise. These strategies aim to provide an additional CHO source for the muscle rather than attenuating the depletion of existing glycogen stores (7). An alternative approach that could potentially enhance endurance exercise capacity would be to utilize an alternative fuel source to CHO and/or slow its normal rate of use during exercise.

Fat, comprising intramuscular triglyceride (IMTG), blood lipids, and adipose tissue is abundant: even the leanest athlete is capable of fueling low- to moderate-intensity exercise lasting at least several days from endogenous fat stores. Paradoxically, one of the classic responses to endurance training is that well-trained athletes have a greater capacity to oxidize fat during submaximal exercise compared with their untrained counterparts (8). Adapting these athletes, who already have the metabolic machinery (i.e., mitochondrial density) to utilize fat at high rates during exercise, to a high-fat diet (“fat loading”) has recently been suggested as a possible strategy to further augment rates of fat oxidation (13). This paper critically evaluates the results of investigations that have examined the effects of fat-adaptation strategies in well-trained endurance or ultra-endurance athletes on substrate metabolism and exercise capacity. We will focus on fat-adaptation protocols lasting <14 d to distinguish between the acute preparation for a single competition event and the effects of longer-term dietary protocols on training responses and adaptations (19). Studies that have employed moderate dietary manipulations will not be discussed.


The effect of consuming a high-fat, low-CHO diet for 1–3 d is to lower resting muscle and liver glycogen stores (2). Such ingestion regimens lead to a reduced rate of whole-body CHO oxidation (i.e., a lowered respiratory exchange ratio [RER]) during subsequent exercise (6). There is clear evidence that short-term “fat loading” is detrimental to endurance capacity and the performance of prolonged exercise (2,6,10,28,32). This impairment in performance is likely to result from a combination of the premature depletion of (lowered) muscle glycogen stores and the absence of any worthwhile increase in the capacity for fat utilization during exercise to compensate for the reduction in available CHO fuel. The results of studies in which short-term fat-adaptation protocols have been undertaken in well-trained individuals are summarized in Table 1.

Effect of 1- to 3-d high-fat, low-CHO diets on endurance performance in well-trained subjects.


There is evidence that a longer period (>7 d) of adherence to a high-fat, low-CHO diet causes metabolic adaptations that substantially enhance rates of fat oxidation during exercise and, to a large extent, compensate for the reduced CHO availability. In fact, a notion among many “popular” diet books is that “fat loading” strategies enhance performance capabilities of endurance and ultra-endurance athletes by making them better able to “tap into body fat stores” (31). Studies employing both direct and indirect techniques to measure rates of substrate utilization in which trained individuals have performed submaximal exercise after long-term fat-adaptation have reported markedly higher rates of fat oxidation compared with consumption of isoenergetic high-CHO diets (11,24,26,27). These investigations also purport to show reduced rates of muscle glycogen use (11,24,27), although these claims are unsubstantiated (see below).

Yet, despite the widespread publicity for “fat loading,” there are few studies in which this strategy has been tested in well-trained subjects (see Table 2). Examination of results of early investigations reveal that the data often fail to support a (proposed) performance benefit. Furthermore, there are often methodological/design flaws that require a conservative and cautious interpretation of the results. In perhaps the best-publicized investigation, Phinney et al. (27) had five well-trained cyclists (V̇O2max 64 mL·kg−1·min−1) ride to exhaustion at ∼65% of V̇O2max before and after 4 wk of adaptation to a high-fat (70% E), low-CHO (<20 g·d−1) diet. This study is frequently cited in support of performance enhancement after fat-loading, despite subjects achieving similar endurance times under both experimental conditions. However, the group results were skewed by an abnormally large improvement in the performance of one cyclist: the remaining four subjects showing little change or indeed an impairment in exercise capacity after the high-fat treatment. Furthermore, in that study (27), the treatment was applied with an order effect—all subjects were tested first with their usual (CHO-rich) diet, followed by the high-fat treatment. Finally, because the cycling test was undertaken at a fixed submaximal workload only equivalent to the exercise intensity at which ultra-endurance events would be performed (16), it is difficult to apply the results from this study to endurance events conducted at higher intensities or self-paced performances involving sprints, such as those seen in the real-life world of sport.

Effect of 5–28 d high-fat, low-CHO diets on endurance and ultra-endurance performance in well-trained subjects.

The second study of fat-adaptation in trained individuals employed a cross-over design to investigate the effects of 2 wk isoenergetic high-fat (70% E) or high CHO (70% E) diet on the capacity to perform a battery of unorthodox exercise protocols (24). After fat-adaptation, subjects were able to cycle longer during a moderate-intensity endurance test to exhaustion (24). However, because this test was undertaken immediately after the completion of two separate high-intensity cycling tests (a 30-s Wingate test and a subsequent intense ride to exhaustion at 90% V̇O2max), it is difficult to isolate the effects of the dietary treatment from the contaminating effects of the preceding performance tests. Furthermore, it is hard to relate the results of the total test battery to real-life sporting conditions. In a separate study from another laboratory, 7-d adaptation to a high-fat, low-CHO diet was associated with a dramatic reduction in cycling time to fatigue at a submaximal workload in moderately trained female cyclists (26).

Finally, a recent investigation by Goedecke et al. (11) also failed to find performance benefits after a high-fat diet compared with an isoenergetic high-CHO diet when matched groups of well-trained subjects followed a 2-wk dietary protocol (Table 2). A major finding from that study, however, was that rates of fat oxidation during submaximal exercise were increased after just 5 d of a high-fat diet (11). This is an important finding of practical significance because it suggests that trained individuals can achieve metabolic shifts toward increased utilization of fat during exercise after relatively short periods of dietary periodization. If high-fat diets can be demonstrated to be an effective strategy for performance enhancement for athletes, then brief (5 d) dietary exposure is far more practical and better tolerated by most subjects than more prolonged periods of intervention.


A number of studies have reported that adaptation to high-fat diets result in glycogen “sparing” during submaximal exercise (11,24,27). However, this observation can, for the most part, be explained as an artifact of the significantly lower resting preexercise muscle glycogen levels seen after consumption of high-fat (compared with high-CHO) diets. True differences in the rate of glycogen utilization during a standardized exercise bout can only be substantiated if subjects start exercise with similar muscle glycogen stores after both high-fat and high-CHO dietary intakes. In such a scenario, the restoration of muscle glycogen stores after a period of fat-loading could, theoretically, confer an athlete the opportunity to enhance fuel provision during exercise from both glycolytic and lipolytic pathways (16). Indeed, it has been previously proposed that optimal endurance and/or ultra-endurance performance could be attained if an athlete trains for most of the year on a high-CHO diet, then undergoes a short (5-d) period of fat-adaptation followed by a period of high-CHO intake to restore muscle and liver glycogen levels (14). Such “dietary periodization” is aimed to enhance the contribution from fat to oxidative metabolism during exercise sparing muscle glycogen, without compromising preexercise endogenous CHO stores (14). In this regard, we have recently undertaken a series of independent, but related, studies investigating this model of dietary periodization (3–5). The results from these studies are summarized in Table 3.

Effect of adaptation (5–10 d) to high-fat, low-CHO diet followed by CHO restoration on endurance and ultra-endurance performance of trained subjects.

The first three studies (3–5) utilized either a 5- or 6-d period of fat-adaptation, followed by a 24-h period of high-CHO intake (i.e., CHO restoration). Trained competitive endurance and ultra-endurance athletes were supervised so that they completed an identical training program (15–22 h·wk−1 of cycling) on each dietary treatment. Measurement of muscle glycogen after 5 d of the high-fat diet showed a lowering of CHO stores compared with the high-CHO diet (255 vs 464 mmol·kg−1 dry weight;3). However, 1 d of rest in combination with a high-CHO diet was sufficient to super-compensate muscle glycogen concentrations (554 vs 608 mmol·kg−1 dry weight for high-fat and high-CHO, respectively), independent of the preceding diet (3). Accordingly, subjects commenced exercise on d 7 with similar glycogen stores. In a fourth study undertaken by Lambert and coworkers (25), a 10-d period of fat adaptation was followed by a 3-d glycogen loading protocol. These four investigations (3–5,25) all determined the effects of dietary interventions on performance using exercise tests that incorporated a portion of steady-state cycling (in which metabolic responses to exercise were determined), followed by a self-paced time-trial (TT) that allowed the subjects to “compete” in a situation that mimics the demands of a real-life sporting event.

Despite the brevity of the adaptation period in each study, fat-adaptation was associated with substantially higher rates of fat oxidation during submaximal exercise (Table 3). Higher rates of fat oxidation persisted even under conditions in which CHO availability was increased either by having athletes consume a high-CHO meal before commencing exercise (4) and/or ingesting glucose solutions during the ride (4,5,25). Thus, the fat-adaptation treatments employed caused powerful metabolic adaptations that were independent of both endogenous and exogenous CHO availability (see Fig. 1). Muscle biopsy techniques (3) and glucose tracer methodology (3,5) showed that the reduction in total CHO oxidation during exercise was almost entirely accounted for by a true sparing of muscle glycogen stores. Other findings included similar rates of utilization of total blood oxidation (3,5) and exogenous (ingested) glucose oxidation (5) throughout exercise after both high-fat and high-CHO diets.

Effect of 5-d adaptation to high-fat diet and 1-d CHO restoration (FAT-adapt) on rate of CHO oxidation and rate of fat oxidation during cycling at 70% V̇O2max compared with control trial (HCHO). Values are mean ± SEM for eight subjects at day 1 (baseline), day 6 (after fat adaptation), and during 120 min of steady-state cycling on day 7 (after fat adaptation and glycogen restoration). Data from two studies: HCHO + CHO and FAT-adapt + CHO to denote intake of CHO before and during cycling on day 7 (4). HCHO − CHO and FAT-adapt − CHO to denote no further intake of CHO on day 7 (3).

It is interesting to note that fat-adaptation strategies induce large increases in rates of whole-body fat oxidation during exercise, even in highly trained individuals who already have an enhanced capacity for fat oxidation (3–5,11,24,25,27). At present, we are unable to determine whether these metabolic changes involve up-regulation of fat oxidation during exercise, a down-regulation of CHO oxidation or, most likely, a combination of both. In this regard, other studies in humans have reported changes in the activity of β-hydroxyacyl-CoA-dehydrogenase (20), cartinine palmitoyl transferase I (9), and pyruvate dehydrogenase (29) after several days or weeks of a high-fat, low-CHO diet. Whether these and/or other changes occur over the period of fat exposure in studies of highly trained athletes who maintain their intense training programs warrants further investigation. Other studies have found that exposure of trained subjects to 1–28 d of a high-fat intake increases IMTG stores (22,23,32). Increased IMTG stores after a period of a high-fat diet may provide an additional substrate pool to account for some or all of the additional fat oxidized after fat-adaptation. The failure to measure IMTG utilization in all investigations of fat-adaptation and dietary periodization (Table 3) is a glaring omission. However, such an oversight can be partially explained by the technical difficulties encountered in making precise measurements of this substrate or its utilization, and the lack of agreement in results produced by direct and indirect measurements of IMTG use during exercise (35).

It is perplexing that in the face of marked changes in metabolism that favor fat oxidation and the consequent sparing of muscle glycogen, fat-adaptation/CHO restoration strategies do not provide clear benefits to the performance of prolonged exercise. Performance differences are minimal in the case of endurance events, especially when they are undertaken with optimal CHO availability (4), but there is some evidence of enhanced performance over longer or ultra-endurance events (5). Several possibilities might help explain the lack of clear benefit to performance from the results of the studies reviewed. First, there may be no actual enhancement in the capacity to undertake prolonged submaximal exercise after high-fat diets in well-trained subjects. Alternatively, the aggressive CHO intake strategies during endurance and ultra-endurance events (i.e., consuming sports drinks, sports gels, and other CHO-rich foods) are sufficient to achieve optimal performance. On the other hand, even though subjects were all highly trained and well-accustomed to riding in laboratory trials in the majority of studies, it is possible that the reliability of time-trials undertaken at the end of long steady-state “preloads” is not sufficiently sensitive to detect the small but real performance improvements. Future studies should endeavor to use performance protocols with high reliability, and employ sufficiently large sample sizes to allow worthwhile changes in performance to be detected (21).

Two other theories merit further discussion. First, there is large interindividual variability to fat-adaptation strategies, with some athletes being “responders” and showing true performance benefits from the treatment, and others being “nonresponders” (3,5,27). It is of interest to investigate this phenomenon further in an attempt to try to distinguish true differences in response to fat-adaptation/CHO restoration strategies as distinct from the day-to-day variability in performance. The specific adaptations that underpin favorable changes in performance capacity need to be identified (i.e., genetic markers) and, if possible, surrogate measures to identify athletes who are likely to respond should be sought.

Second, there is strong evidence that fat-adaptation strategies result in a reduced reliance on muscle glycogen utilization during exercise (3), even when muscle CHO content is restored to normal levels or super-compensated (4,5). Such glycogen sparing implies that there may be benefits in prolonging the availability of this otherwise limited fuel store. However, an alternative theory is to consider that fat-adaptation strategies produce impairment in glycogen utilization and a reduced ability to utilize this important fuel source. If this is the case, then fat-adaptation would be expected to compromise the performance of intense exercise (>85% of V̇O2max) where muscle glycogen is the predominant substrate (30,34). Although endurance and particularly ultra-endurance sports are typically characterized as events of prolonged, submaximal, steady-state exercise, successful performers must also be able to sustain intense bouts of exercise to counter sudden and unexpected changes in terrain, the breakaway tactics of other competitors and the sprint to the finish line. Other studies have reported that fat-adaptation strategies have a negative effect on the capacity to perform high-intensity exercise (for review see 18). However, to date, this phenomenon has not been studied systematically in well-trained athletes who have undertaken fat-adaptation/CHO restoration protocols (33).


In summary, the results from a number of studies show that 1–3 d of exposure to a high-fat, low-CHO diet is associated with a lowering of resting muscle (and presumably liver) glycogen stores and a reduction in exercise performance. The impairment in exercise capacity is likely to result from a combination of the premature depletion of (lowered) muscle glycogen stores and the absence of any worthwhile increase in the capacity for fat utilization during exercise to compensate for the reduction in available CHO fuel. Longer periods of adherence to a high-fat diet, however, substantially enhance the capacity for fat oxidation during submaximal exercise, with evidence that the major shifts in the pattern of substrate metabolism (from CHO to fat) can be achieved within 5–6 d. This scenario presents a practical opportunity for enhancement of endurance and/or ultra-endurance performance via dietary manipulation. Studies in well-trained individuals show that fat-adaptation strategies alone do not enhance the performance of prolonged exercise. However, because elevated rates of fat oxidation resulting from high-fat diets are maintained even in the face of acute strategies to promote CHO availability, there is an opportunity to simultaneously enhance the potential for fat and CHO utilization during exercise (i.e., dietary periodization). True glycogen sparing has been demonstrated after fat-adaptation/CHO restoration protocols during prolonged, submaximal cycling exercise. Nevertheless, despite significant glycogen sparing, studies to date have failed to find clear evidence of benefits to the performance of endurance and ultra-endurance exercise following fat-adaptation.

Future studies in this area should focus on examining the possibility that there are “responders” and “nonresponders” to dietary fat-adaptation strategies: determining the underlying mechanisms for this observation and identifying simple markers for this response is more difficult. The effect of fat-adaptation/CHO restoration strategies on the performance of high-intensity exercise has received little scientific attention: if athletes are to benefit from specific nutritional/training regimens, it is necessary that training intensity can be maintained while consuming a high-fat diet. Fine-tuning fat-adaptation/CHO-loading strategies to elucidate the minimal amount of time for adherence to each dietary protocol, the optimal volume and intensity of training to achieve adaptations and prepare for performance, and the number of times that this protocol could be undertaken in the athlete’s macro cycle will require a series of independent studies, as will defining the specific sporting situations and/or exercise protocols that may benefit from fat adaptation/CHO restoration strategies. Manipulating the fatty acid content of athletes’ diets may prove to result in more favorable metabolic profiles during submaximal exercise (i.e., greater rates of fat oxidation). Finally, defining the precise mechanism(s) underpinning some of the observed metabolic perturbations in response to fat-adaptation should provide those exercise physiologists/exercise biochemists with an interest in the regulation of fuel metabolism during exercise occupied for many years.

We wish to acknowledge the contribution of the following individuals in our research team: Dr. Damien Angus, Greg Cox, Nicola Cummings, Dr. Mark Febbraio, Kathryn Gawthorn, Michelle Minehan, Dr. David Martin, Professor Mark Hargreaves, Sally Clark, Ben Desbrow, Andrew Carey, Heidi Staudacher, Nigel Stepto, and Vasilis Nikopoloulos.

Funding for the studies conducted in the authors laboratories was provided by grants from the Sports Science Sports Medicine Center of the Australian Institute of Sport, Kellogg (Australia) Pty Ltd., and Nestle Australia.

Address for correspondence: Louise M Burke, Ph.D., Department of Sports Nutrition, P.O. Box 176, Belconnen, ACT 2616, Australia; E-mail:


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