Journal Logo


Long-term fat diet adaptation effects on performance, training capacity, and fat utilization


Author Information
Medicine & Science in Sports & Exercise: September 2002 - Volume 34 - Issue 9 - p 1499-1504
  • Free


In a paper published some years ago Sherman and Lenders implicated fat loading as “the next magic bullet” in the pursuit of the optimal diet for endurance performance (37). Since then, several studies have investigated whether in fact endurance performance can be enhanced after adaptation to fat-rich diet, a research question that was initially addressed by Christensen and Hansen (5) more than 60 years ago. In this paper, focus is mainly oriented toward long-term adaptation to fat-rich diet, and discussion of short-term adaptation to fat-rich diet is available elsewhere (3,12). Fat adaptation both short and long term induces a markedly higher fat oxidation during exercise and thus a reduced carbohydrate utilization (5,30). Furthermore, when a fat-rich diet is consumed, muscle glycogen is at best maintained and in many cases lower than when compared with consuming a carbohydrate-rich diet (16,30). It is therefore not clear whether the fat-diet–induced carbohydrate sparing is sufficient to counterbalance the lower glycogen storage and thus overall lead to an increased exercise capacity. The present paper will briefly discuss the evidence available on the effect of long-term fat diet adaptation on endurance performance. Subsequently, two questions will be addressed: first, whether in the light of a reduced muscle glycogen storage it is possible to maintain training intensity while consuming a fat-rich diet, and second, which source(s) of fat that contributes to the increased oxidation of fat during submaximal exercise after long-term fat diet adaptation.


When evaluating the effect of fat-rich diet on endurance performance after long-term fat diet adaptation, there is a range of factors, such as duration of the dietary period, the fat and carbohydrate content of the diets, the exercise intensity at which performance is measured, and the training status of the subjects, all of which can influence the performance outcome (12). Here focus is narrowed down to high-fat diets (>40% fat), consumed for 10 d or longer and with exercise intensity of the time to exhaustion performance test between 60 and 85% of maximal oxygen uptake (V̇O2max). In addition, two studies where time trials were used after long-term fat diet adaptation was included. The exercise intensity range of 65–85% of V̇O2max was selected because muscle glycogen is considered to play a key role in fatigue at these intensities (17,34,35). Within the criteria given above, the majority of studies do not find any difference in endurance performance when adaptation to fat- and carbohydrate-rich diets is compared (6,11,16,19,26,30,31)(Table 1). However, a study by Lambert and colleagues (25) demonstrated that endurance performance at 60% of V̇O2max was significantly higher after 14-d adaptation to fat-rich diet, containing 70% fat, than when compared with carbohydrate-rich diet. But in their study, endurance testing was preceded both by a Wingate test and exercise at 90% of V̇O2max until exhaustion, and these data should therefore be carefully interpreted. Furthermore, a recent study found an increased endurance performance after 28 d adaptation to a 41% fat diet when compared with a carbohydrate diet (18) (Table 1). However, in this study by Hoppeler et al. (18) where a crossover design was implemented energy intake was 21% lower during the low-fat diet compared with the fat diet, but body mass and body fat content were not affected differently after the two diets. This may imply that energy intake was not optimal and maybe even deficient during the low-fat diet, and this could have attenuated performance. On the other hand, there is some evidence that fat-rich diet can be detrimental for exercise performance. Pruett (32) demonstrated that exercise endurance performance at 70% of V̇O2max was clearly attenuated after 14 d adaptation to a fat-rich diet compared with after a carbohydrate-rich diet. Using a different exercise model, Simonsen et al. (38) demonstrated that rowing performance, measured as average power output across three rowing time trials over 2500 m separated by 8 min, was impaired after 28 d adaptation to a fat diet containing 42% of energy as fat compared with carbohydrate diet (Table 1). In a more recent study, it was demonstrated that when untrained subjects participated in a regular training program for 7 wk while consuming either a fat or a carbohydrate diet, the endurance performance was markedly attenuated after the fat diet (14). In a later study where a similar design was applied, almost identical data were obtained, showing a significant attenuation of endurance performance after 7 wk adaptation to fat diet and training (N = 7) when compared with adaptation to carbohydrate diet and training (N = 6) (Fig. 1, author’s unpublished data). A recently published pilot study (only 3 subjects) by Lukaski et al. (26) demonstrated a decreased endurance performance at 70–75% of V̇O2max after 28 d adaptation to polyunsaturated fat-rich diet compared with both saturated fat-rich diet and carbohydrate-rich diet. Further studies are needed to address whether indeed endurance performance outcome is significantly affected by the dietary fatty acid composition of high-fat diets. Thus, overall, there is evidence to suggest that endurance performance at best can only be maintained after long-term adaptation to fat-rich diets when compared with carbohydrate-rich diets, and based on this, long-term fat diet usage cannot be recommended.

Endurance performance after long-term fat dietadaptation.
Time to exhaustion at 71% maximal oxygen uptake before and after 7-wk adaptation to training and either a fat or a carbohydrate diet. Results are mean ± SE (author’s unpublished findings). * (P < 0.05) initial vs 7 wk; † (P < 0.05) fat diet vs carbohydrate-rich diet.


In the literature, muscle glycogen is considered to play a key role in fatigue when exercise intensity ranges between 65 and 85% of V̇O2max (17,34,35). Based on this fact, fat-rich diet adaptation have been used in an attempt to spare muscle glycogen and decrease carbohydrate oxidation and thus hypothetically optimize performance. Unfortunately, this carbohydrate sparing after fat diet adaptation is often accompanied by a reduced muscle (30) and liver (20) glycogen storage compared with consumption of a high-carbohydrate diet. Because a prerequisite for an optimal endurance performance is that training both in regards to quality and quantity is optimal, it is not clear whether in fact training intensity can be maintained during a long-term fat-rich diet adaptation.

Interestingly, this question was addressed already more than 70 years ago by Marsh and Murlin (27), who had one subject consume a normal, a high-fat, and a high-carbohydrate diet for 11 d. On most days, the subject undertook one or two light exercise bouts, and the following is the authors description of the subjects ability to handle the exercise during adaptation to the fat diet: “After the first two or three days the subject felt very tired and sleepy, in fact did sleep several hours between experiments, and had no desire to work or to do anything else. The work seemed harder, although actually it was the same as in the previous series. In the last few experiments the subject became dizzy on the ergometer toward the end of the work period and afterward expressed fear that he might have fallen off. But he stuck pluckily until the series was completed. The very last experiment had to be discontinued at the end of 6 2/5 min because of dizziness.” (27). When the subject consumed the carbohydrate diet, all exercise tests were performed without problems. Thus, for this person, training was possible during fat diet adaptation although it did require a higher mental effort.

In three studies performed during the last 7 years, a number of subjects completed a supervised endurance-training program while consuming a fat-rich diet in our lab. In total, 17 subjects performed 7-wk cycle training (4 times a wk) (14,15) and seven subjects performed 4-wk cycle training (4 times a wk) (16) while consuming a fat-rich diet. All this training was supervised in the lab, and exercise intensity ranged between 60 and 85% of V̇O2max (active breaks at 40–50% V̇O2max), and every single training session was completed. Thus, in subjects who were initially untrained to moderately trained regular endurance, training could be tolerated while a fat-rich diet containing some 62% of energy as fat was consumed. However, based on training diaries (personal comments included), it is evident that in many cases a higher mental effort was needed to sustain the scheduled exercise sessions while consuming a fat-rich diet compared with consuming a carbohydrate diet. In one study, the subjective rating of perceived exertion (Borg Scale (2)) was evaluated by the subjects every 15 min until and at exhaustion at the test before and after 7-wk adaptation to fat-rich diet (N = 7) and training or carbohydrate-rich diet (N = 6) and training (Fig. 2, author’s unpublished findings). At the initial test before the initiation of training and diet, there was no difference in subjective rate of exertion, whereas after 7 wk, the exercise was perceived as more strenuous after fat-rich diet than after carbohydrate-rich diet (Fig. 2, author’s unpublished findings). Interestingly, the level of exertion at exhaustion was not different between groups. Direct adverse effects of fat diet during training were sparse, although across all the training sessions reported a few cases of dizziness (3) and vomiting (1) occurred for the subjects adapting to fat-rich diet.

Rate of perceived exertion (Borg Scale) during submaximal exercise until exhaustion before (A) and after 7 wk (B) adaptation to training and either a fat or a carbohydrate diet. Results are mean ± SE (author’s unpublished findings). Exh, exhaustion; * (P < 0.05) fat vs carbohydrate.

In elite-trained subjects, there is only limited evidence available on training capacity while consuming fat-rich diets. In a recent study by Stepto et al. (41), seven elite trained endurance athletes underwent two 4-d dietary periods consuming either a high-carbohydrate diet (70–75% carbohydrate) or a high-fat diet (>65% fat) in a crossover design with an 18-d washout period in between. During the dietary adaptation, subjects performed two controlled exercise sessions on days 1 and 4, where they exercised for 20 min at 65% of V̇O2max and subsequently performed 8 × 5 min exercise bouts at 86% V̇O2max interspersed with 60 s breaks. In addition to the training performed in the lab, the subjects also undertook training outside, but no difference in duration was apparent between dietary periods. The subjects were for all but one high-intensity exercise bout capable of performing the training while consuming the fat-rich diet, but interestingly the subjective rating of perceived exertion was higher on day 4 in the last few bouts after fat-rich diet when compared with the carbohydrate-rich diet. This indicates that at least for 4 d elite athletes are capable of performing training at a reasonably high intensity while consuming a fat-rich diet, although the cost is a higher subjective rate of perceived exertion.

What is then the mechanism for the higher mental effort needed to sustain exercise during fat-rich diet adaptation? Previous studies of short- (10,21) and long-term adaptation (14) to fat-rich diet reveal a significantly higher catecholamine response as well as heart rate during submaximal exercise compared with when a carbohydrate-rich diet was consumed, thus indicating that both short- and long-term fat diet adaptation induces an increased activity in the sympathetic nervous system during exercise. Furthermore, there is evidence that 14 d of low-fat diet adaptation in healthy female subjects lead to an increased parasympathetic response when compared with a diet with a higher fat content (28). Based on the evidence above, it seems likely that a changed autonomic nervous system activity—increased sympathetic and possibly decreased parasympathetic response—due to the fat diet consumption is contributing to the increased perception of exertion experienced during exercise. However, the exact explanation for the coupling between the fat-diet–induced increase in sympathetic response and the increased perception of exertion during submaximal exercise remains to be demonstrated. Obviously, the higher mental strain and in addition the higher heart rate during exercise while consuming a fat-rich diet will imply that exercise intensity needs to be controlled by objective measures such as oxygen uptake or power output to secure that intensity is indeed as requested.


It is well known that adaptation to a fat-rich diet will lead to measurable changes in the capacity to store (in muscle), recruit, transport, and oxidize fat (9,13,23,30). In consequence of these adaptations both short- (5,24) and long-term (14,30) fat diet adaptation leads to an increased fat oxidation during exercise. However, only few studies have actually addressed which fat source(s) that contribute to this increased fat oxidation?

During exercise, fat is recruited for oxidation both from the plasma in the form of free FA (and albumin bound FA) and as very low-density lipoprotein triacylglycerol (VLDL-TG) and from muscle as triacylglycerol either from intra- or extracellular stores (42). In a recent study, Schrauwen and colleagues (36) applied a stable isotope tracer technique to investigate the substrate utilization after 7-d adaptation to either fat-rich (60% fat, 25% carbohydrate) or carbohydrate-rich diet (30% fat, 55% carbohydrate). In their study, the plasma FA oxidation was similar between diets, and therefore it was concluded that the higher fat oxidation (190%) observed during exercise at 50% of Wmax after the fat diet was derived from muscle and/or plasma triacylglycerol (36). In a recently published study (15), we investigated the effect of long-term adaptation to training and either fat rich or carbohydrate-rich diet on substrate utilization during submaximal exercise. After 7-wk adaptation to diet and training, we combined the application of the stable isotope tracer technique with the arteriovenous balance technique (flow determined by thermodilution) during 60 min of submaximal bicycle exercise at 70% of V̇O2max. In addition, we obtained muscle biopsies from m vastus lateralis before and after exercise. By using this approach, it was evident that across the leg the fat-diet–induced increase in fat oxidation was derived from an increased utilization of VLDL-TG (calculated from the Fick principle) and from a stable isotope determined increased utilization of plasma fatty acids (Fig. 3 (15)). We were not able to measure a significant biochemical breakdown of muscle triacylglycerol across the exercise bout and, as such, concluded that muscle triacylglycerol was not a prime contributor to the increased fat oxidation. In contrast to Schrauwen and colleagues (36), we observed increased plasma FA utilization, but this may simply be due to the difference in duration of the dietary period; theirs was 7 d and we used 7 wk and furthermore added training as an intervention. It has previously been demonstrated that FA originating from VLDL-TG contributed to fat oxidation in a trained leg during exercise (22), a finding that is coherent with a fat diet induced increase in muscle lipoprotein lipase activity (23). Thus overall, this suggests that during exercise, fat recruited from both plasma and plasma VLDL-TG, but not muscle triacylglycerol, is responsible for the increased fat oxidation after long-term fat diet adaptation. It is intriguing that muscle triacylglycerol utilization is not increased after a fat diet considering that a high dietary fat content will lead to an increased muscle triacylglycerol storage (16,23) and vice versa a low dietary fat content a decreased muscle triacylglycerol storage (7,40). However, the substrate balance in our recent paper (15) demonstrates that a minor fraction of lipid is unaccounted for, and it is not possible to exclude that this fraction or parts of it could potentially be muscle triacylglycerol. It is important to realize that the issue of muscle triacylglycerol utilization during exercise is controversial. Under normal dietary conditions, several studies originating from independent laboratories using different methodologies could not demonstrate muscle triacylglycerol utilization during exercise (1,22,33,39,40), whereas others found a significant breakdown amounting to approximately 20–35% (4,8,29,36). As such, final conclusions on the role of muscle triacylglycerol during exercise after fat diet adaptation must be left for future studies and the advent of a very precise analysis method.

Contribution of blood and muscle derived substrates to total fuel oxidation in the leg during exercise in the fasted state after 7 wk of training and adaptation to either a fat or a carbohydrate diet. The substrate contribution from muscle glycogen was determined as net breakdown multiplied by the estimated active muscle mass of the leg (4 kg) (modified from (15)). Values are means. * (P < 0.05) fat diet vs carbohydrate diet.


Overall, there is evidence to suggest that endurance performance at best can only be maintained after long-term adaptation to fat-rich diets when compared with carbohydrate-rich diets, and therefore long-term fat diet usage cannot be recommended as a tool to improve endurance performance. There is good evidence that a reasonably high training intensity was possible over prolonged periods of fat diet consumption in untrained to moderately trained subjects, and that high intensity interval training could be tolerated by elite athletes during short-term fat-rich diet adaptation. However, in both untrained, moderately trained, and elite athletes, a higher mental effort was required to perform the exercise training, possibly due to a fat-diet–induced higher sympathetic nervous activation. This necessarily implies that if fat diet adaptation is applied under “free living conditions,” it will be very important to secure that training intensity is not decreased due to the higher “stress” level. Unfortunately, there is still a clear lack of mechanistic understanding both in relation to performance and in relation to metabolic adaptation after prolonged fat diet adaptation, and further studies are necessary before more final conclusions are possible.

In perspective.

Already more than 80 years ago, Krogh and Lindhard (24) studied the effects of dietary manipulations on substrate utilization during exercise. In that study, six subjects (including Krogh and Lindhard) participated in a crossover design in which a 3-d very-high-fat or very-high-carbohydrate diet was consumed. Exercise was performed on the Krogh bicycle ergometer and the following is the author’s observations on the effect of diet on fatigue. “1. The fatigue at different quotients. The subjects J.L, G.L, A.K., and O.H. observed distinct differences in the facility (or difficulty) with which the prescribed amount of work was performed, coincident with changes in diet and noted that on fat diets the fatigue became considerable and sometimes excessive. For several hours after the work on the ergometer these subjects were generally very tired.... The subjects R.E. and A.M.N. failed to observe any appreciable difference between work on the two diets.” (24). A similar divergent individual performance response after prolonged adaptation to a very high fat diet can be found in a paper by Phinney and Colleagues (30), and although we now 80 years after can explain a large part of the biochemical adaptations behind the adaptations observed by Krogh and Lindhard (24), there is to the best of my knowledge still not solid evidence to explain these individual differences. Thus, future studies should address whether indeed there is such an individual response to high fat diets and subsequently provide the physiological explanation behind a such difference.

The author and the experimental work performed by the author was supported by grants from the Danish Research Academy, Per Henriksens Fond, Team Danmark, the Danish Sports Research Council, and Danish National Research Foundation grant no. 504-14.

Address for correspondence: Jørn Wulff Helge, Copenhagen Muscle Research Centre, H:S State Hospital, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark;


1. Bergman, B. C., G. E. Butterfield, E. E. Wolfel, G. A. Casazza, G. D. Lopaschuk, and G. A. Brooks. Evaluation of exercise and training on muscle lipid metabolism. Am. J. Physiol. 276: E106–E117, 1999.
2. Borg, G. A. V. Psychophysical bases of perceived exertion. Med. Sci. Sports Exerc. 14: 377–382, 1982.
3. Burke, L. M., and J. A. Hawley. Effects of short-term fat adaptation on metabolism and performance of prolonged exercise. Med. Sci. Sports Exerc. 34: 1492–1498, 2002.
4. Carlson, L. A., L. G. Ekelund, and S. O. Froberg. Concentration of triglycerides, phospholipids and glycogen in skeletal muscle and of free fatty acids and beta-hydroxybutyric acid in blood in man in response to exercise. Eur. J. Clin. Invest. 1: 248–254, 1971.
5. Christensen, E. H., and O. Hansen. Arbeitsfähigkeit und Ernärung (Work capacity and dietary intake). Skand. Arch. Physiol. 81: 160–171, 1939.
6. Cox, C. M., R. C. Brown, and J. I. Mann. The effects of high-carbohydrate versus high-fat dietary advice on plasma lipids, lipoproteins, apolipoproteins, and performance in endurance trained cyclists. Nutr. Metab. Cardiovasc. Dis. 6: 227–233, 1996.
7. Coyle, E. F., A. E. Jeukendrup, M. C. Oseto, B. J. Hodgkinson, and T. W. Zderic. Low-fat diet alters intramuscular substrates and reduces lipolysis and fat oxidation during exercise. Am. J. Physiol. Endocrinol. Metab. 280: E391–E398, 2001.
8. Essen, B., L. Hagenfeldt, and L. Kaijser. Utilization of blood-borne and intramuscular substrates during continuous and intermittent exercise in man. J. Physiol. (Lond.) 265: 489–506, 1977.
9. Fisher, E. C., W. J. Evans, S. D. Phinney, G. L. Blackburn, B. R. Bistrian, and V. R. Young. Changes in skeletal muscle metabolism induced by a eucaloric ketogenic diet. In: H. G. Knuttgen, J. A. Vogel, and J. Portman (Eds.). Champaign, IL: Human Kinetics, 1983, pp. 497–501.
10. Galbo, H., J. J. Holst, and N. J. Christensen. The effect of different diets and of insulin on the hormonal response to prolonged exercise. Acta Physiol. Scand. 107: 19–32, 1979.
11. Goedecke, J. H., C. Christie, G. Wilson, et al. Metabolic adaptations to a high-fat diet in endurance cyclists. Metabolism 48: 1509–1517, 1999.
12. Helge, J. W. Adaptation to a fat-rich diet: effects on endurance performance in humans. Sports Med. 30: 347–357, 2000.
13. Helge, J. W., and B. Kiens. Muscle enzyme activity in man: role of substrate availability and training. Am. J. Physiol. 272: R1620–R1624, 1997.
14. Helge, J. W., E. A. Richter, and B. Kiens. Interaction of training and diet on metabolism and endurance during exercise in man. J. Physiol. (Lond.) 292: 293–306, 1996.
15. Helge, J. W., P. W. Watt, E. A. Richter, M. J. Rennie, and B. Kiens. Fat utilization during exercise; adaptation to fat rich diet increases utilization of plasma FA and VLDL-TG. J. Physiol. 537: 1009–1020, 2001.
16. Helge, J. W., B. Wulff, and B. Kiens. Impact of a fat rich diet on endurance in man: Role of the dietary period. Med. Sci. Sports Exerc. 30: 456–461, 1998.
17. Hermansen, L., E. Hultman, and B. Saltin. Muscle glycogen during prolonged severe exercise. Acta Physiol. Scand. 71: 129–139, 1967.
18. Hoppeler, H., R. Billeter, P. J. Horvath, J. J. Leddy, and D. R. Pendergast. Muscle structure with low- and high-fat diets in well-trained male runners. Int. J. Sports Med. 20: 522–526, 1999.
19. Horvath, P. J., C. K. Eagen, N. M. Fisher, J. J. Leddy, and D. R. Pendergast. The effects of varying dietary fat on performance and metabolism in trained male and female runners. J. Am. Coll. Nutr. 19: 52–60, 2000.
20. Hultman, E., and L. Nilsson. Liver glycogen in man: effect of different diets and muscular exercise. In: Muscle Metabolism During Exercise, B. Pernow and B. Saltin (Eds.). New York: Plenum, 1971, pp. 143–151.
21. Jansson, E., P. Hjelmdahl, and L. Kaijser. Diet induced changes in sympatho-adrenal activity during submaximal exercise in relation to substrate utilization in man. Acta Physiol. Scand. 114: 171–178, 1982.
22. Kiens, B., B. Essen-Gustavsson, N. J. Christensen, and B. Saltin. Skeletal muscle substrate utilization during submaximal exercise in man: effect of endurance training. J. Physiol. (Lond.) 469: 459–478, 1993.
23. Kiens, B., B. Essen-Gustavsson, P. Gad, and H. Lithell. Lipoprotein lipase activity and intramuscular triglyceride stores after long term high-fat and high-carbohydrate diets in physically trained men. Clin. Physiol. 7: 1–9, 1987.
24. Krogh, A., and J. Lindhard. The relative value of fat and carbohydrate as sources of muscular energy. Biochem. J. 14: 290–363, 1920.
25. Lambert, E. V., D. P. Speechly, S. C. Dennis, and T. D. Noakes. Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet. Eur. J. Appl. Physiol. 69: 287–293, 1994.
26. Lukaski, H. C., W. W. Bolonchuk, L. M. Klevay, D. B. Milne, and H. H. Sandstead. Interactions among dietary fat, mineral status, and performance of endurance athletes: a case study. Int. J. Sport Nutr Exerc. Metab. 11: 186–198, 2001.
27. Marsh, E., and J. R. Murlin. Muscular efficiency on high carbohydrate and high fat diets. J. Nutr. 1: 105–137, 1928.
28. Pellizzer, A. M., N. E. Straznicky, S. Lim, P. W. Kamen, and H. Krum. Reduced dietary fat intake increases parasympathetic activity in healthy premenopausal women. Clin. Exp. Pharmacol. Physiol. 26: 656–660, 1999.
29. Phillips, S. M., H. J. Green, M. A. Tarnopolsky, G. F. Heigenhauser, R. E. Hill, and S. M. Grant. Effects of training duration on substrate turnover and oxidation during exercise. J. Appl. Physiol. 81: 2182–2191, 1996.
30. Phinney, S. D., B. R. Bistrian, W. J. Evans, E. Gervino, and G. L. Blackburn. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 32: 769–776, 1983.
31. Pogliaghi, S., and A. Veicsteinas. Influence of low and high dietary fat on physical performance in untrained males. Med. Sci. Sports Exerc. 31: 149–155, 1999.
32. Pruett, E. D. R. Glucose and insulin during prolonged work stress in men living on different diets. J. Appl. Physiol. 28: 199–208, 1970.
33. Rico-Sanz, J., J. V. Hajnal, E. L. Thomas, et al. Intracellular and extracellular skeletal muscle triglyceride metabolism during alternating intensity exercise in humans. J. Physiol. (Lond.) 510: 615–622, 1998.
34. Romijn, J. A., E. F. Coyle, L. S. Sidossis, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am. J. Physiol. 265: E380–E391, 1993.
35. Saltin, B., and J. Karlsson. Muscle glycogen utilization during work at different intensities. Adv. Exp. Med. Biol. 11: 289–299, 1971.
36. Schrauwen, P., A. J. Wagenmakers, W. D. Marken Lichtenbelt, W. H. Saris, and K. R. Westerterp. Increase in fat oxidation on a high-fat diet is accompanied by an increase in triglyceride-derived fatty acid oxidation. Diabetes 49: 640–646, 2000.
37. Sherman, W. M., and N. Leenders. Fat loading: the next magic bullet. Int. J. Sport Nutr. 5: S1–S12, 1995.
38. Simonsen, J. C., W. M. Sherman, D. R. Lamb, A. R. Dernbach, J. A. Doyle, and R. Strauss. Dietary carbohydrate, muscle glycogen, and power output during rowing training. J. Appl. Physiol. 70: 1500–1505, 1991.
39. Standl, E., N. Lotz, T. Dexel, H.-U. Janka, and H. J. Kolb. Muscle triglycerides in diabetic subjects: Effects of insulin deficiency and exercise. Diabetologica 18: 463–469, 1980.
40. Starling, R. D., T. A. Trappe, A. C. Parcell, C. G. Kerr, W. J. Fink, and D. L. Costill. Effects of diet on muscle triglyceride and endurance performance. J. Appl. Physiol. 82: 1185–1189, 1997.
41. Stepto, N. K., D. T. Martin, K. E. Fallon, and J. A. Hawley. Metabolic demands of intense aerobic interval training in competitive cyclists. Med. Sci. Sports Exerc. 33: 303–310, 2001.
42. Turcotte, L. P. Role of fats in exercise: types and quality. Clin. Sports Med. 18: 485–498, 1999.


©2002The American College of Sports Medicine