JACN Did you know that you can get alerts when a new issue is online?
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Horvath, P. J.
Right arrow Articles by Pendergast, D. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Horvath, P. J.
Right arrow Articles by Pendergast, D. R.
Journal of the American College of Nutrition, Vol. 19, No. 1, 52-60 (2000)
Published by the American College of Nutrition


Original Research

The Effects of Varying Dietary Fat on Performance and Metabolism in Trained Male and Female Runners

Peter J. Horvath, PhD, FACN, CNS, Colleen K. Eagen, MS, Nadine M. Fisher, EdD, John J. Leddy, MD and David R. Pendergast, EdD

Departments of Physical Therapy, Exercise & Nutrition Sciences and Physiology and The Sports Medicine Institute, University at Buffalo, Buffalo, New York

Address reprint requests to: Dr. Peter J. Horvath, 15 Farber Hall, Nutrition Program, Department of Physical Therapy, Exercise and Nutrition Sciences, University at Buffalo, Buffalo, NY 14214.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Objectives: Low dietary fat intake has become the diet of choice for many athletes. Recent studies in animals and humans suggest that a high fat diet may increase o2 max and endurance. We studied the effects of a low, medium and high fat diet on performance and metabolism in runners.

Methods: Twelve male and 13 female runners (42 miles/week) ate diets of 16% and 31% fat for four weeks. Six males and six females increased their fat intakes to 44%. All diets were designed to be isocaloric. Endurance and O2 max were tested at the end of each diet. Plasma levels of lactate, pyruvate, glucose, glycerol, and triglycerides were measured before and after the O2 max and endurance runs. Free fatty acids were measured during the O2 max and endurance runs.

Results: Runners on the low fat diet ate 19% fewer calories than on the medium or high fat diets. Body weight, percent body fat (males=71 kg and 16%; females=57 kg and 19%), O2 max and anaerobic power were not affected by the level of dietary fat. Endurance time increased from the low fat to medium fat diet by 14%. No differences were seen in plasma lactate, glucose, glycerol, triglycerides and fatty acids when comparing the low versus the medium fat diet. Subjects who increased dietary fat to 44% had higher plasma pyruvate (46%) and lower lactate levels (39%) after the endurance run.

Conclusion: These results suggest that runners on a low fat diet consume fewer calories and have reduced endurance performance than on a medium or high fat diet. A high fat diet, providing sufficient total calories, does not compromise anaerobic power.

Key words: O2 max, endurance, expiratory gas exchange ratio, dietary fat intake, fat oxidation, lactate, runners


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
The availability of energy is essential to the performance of athletes. Energy availability has two components: the first is the rate of availability, which determines the athlete’s power output; the second is the availability of substrate to supply energy over the exercise time. These two factors together are important determinants of athletic performance.

The rate of energy supply for prolonged exercise is dependent upon the maximal aerobic power. There is a strong relationship between performance and O2 max in endurance athletes [1]. The O2 max of an individual athlete can be improved by training [1]. In addition, recent studies in animals and man have also shown that O2 max can be increased in trained subjects by increasing dietary fat intake [2,3,4].

Endurance performance also depends on the rate of utilization of glycogen and fats and the quantity of their storage in the muscle. The depletion of muscle glycogen stores during endurance exercise has been correlated to fatigue [5], and moderate to high intensity exercise has been found to be enhanced by a carbohydrate sufficient diet [5,6]. Increasing the percent of carbohydrates in the diet, termed "carbohydrate loading," has been shown in some athletes to improve performance [5]. These studies [5,6] used untrained subjects or trained subjects whose caloric intake was less than their expenditure. This low caloric and high carbohydrate intake is typical of many endurance runners [7]. If caloric intake is low, glycogen and fat stores may be compromised. In this setting, increasing carbohydrate intake may therefore improve performance.

Highly trained endurance athletes have an increased ability to oxidize fats and thus spare glycogen [8,9]. Previous studies have reported that, as exercise intensity increases, glycogen use increases as indicated by a higher expiratory gas exchange ratio (R) [1]. The R is lower, indicating greater fat utilization, at a given O2 max or percent of O2 max in trained runners [1]. Some studies have shown that increasing the fat intake of athletes may reduce performance [5]. These studies, however, used unfit or energy-deficient athletes either who could not increase oxidation of fat or whose glycogen stores were compromised as fat intake increased.

The oxidative capacity of muscle has been shown to improve after training via increases in the number of mitochondria and the quantity of enzymes involved in fat oxidation [10,11]. Fat stores in the adipose tissue are extensive; however, their transport and thus their use is limited [12]. Intramuscular fat stores, particularly those in contact with mitochondria, may be limited in athletes with low fat intakes due either to a low percentage of dietary fat or to low total caloric intakes [12]. It has been shown in an animal model that increasing dietary fat intake can increase the number of mitochondria and fat stores in the muscle [13]; it is reasonable to hypothesize this may apply to humans as well.

The purpose of this study was to determine if increasing dietary fat intake from the low levels (about 15% of daily calories) typical of runners to higher levels (about 45% of daily calories), while maintaining adequate levels of carbohydrates, increased O2 max and endurance time. Furthermore, the total body metabolism of fats and carbohydrates was measured to examine the potential mechanisms involved.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Subjects
Thirteen hundred runners from the greater Buffalo metropolitan area running community were sent letters requesting their participation in this study. Forty-five subjects meeting the criteria below were asked to participate. The Institutional Review Board on Human Subjects and Experimentation at the University at Buffalo approved this project and the subjects signed informed consent. The subjects were screened using the following criteria: minimum training of 35 miles per week, healthy, non-smoking and between the ages of 18 and 55 years. Twelve males and thirteen females completed the first two diet periods and six males and six females completed all three diets. Therefore, comparisons were made using all 25 subjects between the first two diets and using 12 subjects between the last two diets. Table 1 describes the physical characteristics of the subjects. Body weight was measured on an electronic scale (Toledo, Model 8142) and their percent of body fat was determined by underwater densitometry [1].


View this table:
[in this window]
[in a new window]
 
Table 1. Subject Characteristics Used for the Low to Medium and for the Medium to High Fat Diet Comparisons

 
Dietary Protocol
Subjects were prescribed three types of diets consisting of seven days of sample menus. The diets varied in fat level and were prepared from three-day food intake records (three-day recall), a food preference list and personal consultation. Auto-Nutritionist IV (First Databank, San Bruno, CA) was used to generate the three diets replacing carbohydrate calories with fat calories. The diets were developed so that the resulting self-selected diets would be of a low, medium and a high fat type, about 15%, 30% and 45% of calories as fat, respectively. The subjects were given the diets as examples, but they selected their own food on the three different diets. They were taught how to record their food, fluid and supplement intake and were requested to complete the records daily and return them weekly for periodic review by the dietitians to determine compliance. Exercise testing was performed at the beginning of the experiment as familiarization and then at the end of each diet, each of which lasted 28 to 31 days. In addition, O2 max testing was done three months after the last diet to evaluate the effects of three months of training per se on performance.

Exercise Protocol
The subjects performed two sets of tests at each testing time. The Wingate Anaerobic Power Test [14] and the O2 max were performed on one day, and then a run to exhaustion at 80% of O2 max was performed on a separate day at least two days and not more than one week apart. Before each test, the average of three measurements taken two minutes apart for blood pressure (Infersonic 2000) and heart rate (ECG Quinton, Q-750) were taken after a 15 minute rest.

The Wingate test [14] was performed on a stationary bike (Monark, Model 868) before the O2 max test. The subjects warmed up for two minutes at 30% to 40% of O2 max. Then the subjects were asked to cycle as fast as they could for the next thirty seconds against a load based on their body weight. The speed was recorded and the external power calculated (load · rpm) every five seconds during the test. The peak (first 5 sec) and average power (over the 30 sec) were calculated. The O2 max test consisted of a three minute period on a treadmill at a zero grade at 6 mph for females and 7 mph for males (training paces) with the grade being increased by 2% every two minutes thereafter until voluntary exhaustion.

All of the endurance test exercise levels were based on the O2 max values obtained before the diet portion of the study. Subjects walked for five minutes at about 30% of their O2 max, and then the speed was increased to 6 and 7 mph at zero grade (40% O2 max) for females and males, respectively. After five minutes, the grade was increased so that each subject was at 60% O2 max for five minutes. After five additional minutes, the subjects were stopped for blood measurement. The subjects then ran at 80% O2 max and ran until voluntary exhaustion.

O2 and CO2 max were measured by collecting expired gas in weather balloons and analyzed by a gas meter (American Meter Co., 802) and mass spectrometry (Perkin-Elmer Medical Instrument Co., Pomona, CA). Gases were collected every two minutes on the O2 max test and every five minutes on the endurance test. The subject’s respiratory exchange ratio (R) was calculated (CO2 · O2-1) for each O2 measurement [2].

Biochemical Parameters
Blood samples were taken from the antecubital vein. Two blood samples were drawn during the O2 max test: one prior to the Wingate test (after a three-hour fast) and another within two minutes after the completion of the O2 max test. Three blood samples were drawn for the endurance test: the first was taken before the exercise was performed (after a three-hour fast), the second 15 minutes after the test started and the last within two minutes after the exercise was completed. Ten to 25 mL of blood was drawn and put into labeled heparinized test tubes with caps. The tubes were then centrifuged at 10,000 rpm for 10 minutes at 4°C. The plasma was then taken off and put into 2 mL micro test tubes and stored at -20°C for later analysis.

Lactate, pyruvate, glycerol, triglyceride and glucose were measured by colorimetric commercial kits (Sigma Diagnostics 228-50, 726, 339-50, and 510-DA) with a Beckman DU 640 spectrophotometer. Free fatty acids were assayed using the spectrophotometric method of Itaya [15]. The only modification was that thirty µL of plasma was mixed with 4 mL chloroform and 1 mL 4% saline solution with 0.05 N hydrochloric acid and left overnight to separate.

Statistical Analysis
The values are expressed as the mean and the standard error of the mean and data was analyzed using NCSS version 6.0 (Kaysville, UT). Two-way ANOVA (GLM) with repeated measures was used with diet and gender as the main factors for all performance data. For blood measurements, a 3-way ANOVA (GLM) with repeated measures was done using diet, gender, and time during the exercise test as the main factors. The effects of the low to medium fat diets were analyzed with an n=25, and the medium to high fat diets were analyzed with an n=12. Post-hoc testing to determine significant difference among the means was done using the Newman-Kuels post-hoc test (p<0.05).


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Dietary Intake and Body Composition
This study was part of a larger study and the detailed dietary intake is reported in the previous paper in this issue. The total daily caloric intake was significantly lower on the low fat diet than on the medium or high fat diets.

The fat levels actually eaten by the runners were 16% and 31% for the 25 subjects used for the low to medium fat diet comparisons and 33% and 44% for the 12 subjects used for the medium and high fat diet comparisons. Protein compositions of the diets were between 13% and 17% for all diets. The percentage of the caloric intake from carbohydrates decreased from the low to medium fat diet; however, total carbohydrate intake was similar due to the increase in total caloric intake on the medium fat diet. Carbohydrate intake declined on the high fat diet compared to the medium and low fat diets, but was never below 250 g/day for the females and 325 g/day for the males. The diets did not change the body weight or percent body fat of the subjects (Table 1).

Metabolism
Maximal Aerobic Power:
There was no change in the maximal grade (8.2 to 7.9) or time to exhaustion by the subjects going from the low and medium fat diets. However, running time was significantly longer on the high than on the medium fat diet (3%), while grade did not significantly increase (8.6 to 8.8). Increasing dietary fat did not change O2 max (expressed per kg), the expiratory gas exchange ratios (which exceeded 1.2 in all tests) or maximal heart rates (Table 2).


View this table:
[in this window]
[in a new window]
 
Table 2. Post O2 max Measurements for Female and Male Runners on Diets of Three Dietary Fat Levels

 
Pre-testing plasma lactate, glucose, pyruvate, and triglyceride (TG) levels were not different on all three diets (Table 5). Posttest lactate levels increased by 11.4 and 11.9 mM on the low and medium fat diets, and 12.4 and 11.3 mM on the medium and high fat diets, respectively. The net lactate accumulation (pretest minus posttest values) was not affected by dietary fat or caloric intake. Plasma glucose and glycerol levels were higher after the O2 max test on all diets. Glucose was 8% higher on the high fat diet compared to the medium fat diet. Plasma triglyceride levels were higher after the O2 max test on the high fat diet.


View this table:
[in this window]
[in a new window]
 
Table 5. Plasma Free Fatty Acid, Triglyceride and Glycerol Levels of Female and Male Runners on Diets of Three Dietary Fat Levels during the Endurance Run

 
Anaerobic Power Test:
Peak power (5th sec) and average power (over 30 sec) were not compromised by increasing the percentage of fat and decreasing the percentage of carbohydrates. Females and males averaged 42 and 58 kpm/sec for peak power and 30.9 and 47.2 kpm/sec for average power, respectively.

Endurance:
The endurance times of the subjects on the medium fat diet increased 20% in females and 8% in males compared to the low fat diet (Table 3). There was no significant difference in endurance time between the high and medium fat diets. There were no significant differences in O2 or heart rate among the three diets as the intensity increased during the test.


View this table:
[in this window]
[in a new window]
 
Table 3. Measurements of Female and Male Runners on Diets of Three Dietary Fat Levels during the Endurance Run

 
The expiratory gas exchange ratio (R=CO2/O2), increased from 0.83 to 0.96 as the workload was increased, but there were no differences in the Rs. Increasing the exercise intensity from 30% to 60% over the first 15 minutes of the endurance test (Table 4 and 5, mid point) did not significantly affect lactate, pyruvate, glucose, triglycerides or free fatty acids, but glycerol levels increased (45% to 50%).


View this table:
[in this window]
[in a new window]
 
Table 4. Plasma Lactate, Pyruvate and Glucose Levels of Female and Male Runners on Diets of Three Dietary Fat Levels

 
After exhaustion, plasma glucose, lactate, pyruvate and glycerol were elevated (Table 4, post). Posttest lactate and pyruvate levels were not different between the low and medium fat diets. However, the subjects had lower posttest lactate (34%) and higher pyruvate on the high fat diet compared to the medium fat diet.


    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
It has been reported that distance runners consume too few calories to meet their energy expenditure and they accomplish this by avoiding fat intake [7]. Therefore, we wanted to determine the effects of increasing dietary fat intake on performance and metabolism in endurance runners. Endurance performance is dependent upon both metabolic power and the available substrates. There is a direct relationship between energy deficits, and reduced glycogen stores and exercise performance [16,17]. Prolonged exercise is carried out at levels below maximal aerobic power by oxidizing a blend of carbohydrates and fats. Glycogen and fat stores are replenished through the diet. A diet that increases dietary fat without compromising glycogen stores has been shown to improve O2 max and endurance performance in endurance athletes [2,6]. In addition, increasing fat consumption increases fat oxidation, which in turn spares glycogen [9,18,19]. Together, these increase O2 max and improve endurance capacity [11]. The blend of glycogen and fats used during exercise is dependent upon exercise intensity and the fitness of the subject [1,5]. Studies showing an improved O2 max and exercise endurance with increased fat intake used a narrow range of fat intake and young male track athletes exercising below 70% of O2 max [2,6,20].

The present study used a wider range of fat intakes, higher intensity endurance exercise, a broader age range of runners and both females and males. To eliminate the training effect on fat oxidation, trained runners were used, thus isolating the effect of dietary fat intake. The runners in this study had been training for a long time and their O2 max and times for 5Ks, 10Ks and marathons did not change across one summer training season (six months). Our results confirmed the improved endurance performance on the medium compared to the low fat diet and that this occurred with women as well as men.

Dietary Intake
The runners did not follow the diets accurately and ate significantly fewer calories on the low fat diet than on the medium or high fat diets. In addition, half of the subjects did not increase their fat intake to the high fat level. The subjects who did not increase their fat intake could have been "fat phobic" or may have had physiological differences such as in their lipoprotein lipase activity [7,21,22]. The levels of fat and caloric intake attained in the present study on the low fat diet are consistent with those of previous studies in athletes [3,10,23]. This has been associated with the runners’ belief that a low body weight is necessary for optimal performance and that fat intake is unhealthy. It has been proposed that on the low fat diet both the caloric restriction and low fat intake result in a reduction in muscle glycogen and fat stores, accounting for the reduced endurance on a low fat diet in both females and males [3,17].

In spite of the increased caloric and fat intake the runners did not gained body weight or adiposity. Studies have shown that energy consumption below predicted expenditures does not result in weight loss in endurance athletes [17,23]. Likewise, increasing caloric intake to meet the demands does not cause a weight gain, but when caloric intake is in excess of caloric expenditure weight gain occurs [1].

Metabolism
Maximal Aerobic Power:
High intensity and prolonged exercise are dependent, in part, on the maximal aerobic power. Metabolic factors play an important role in limiting maximal aerobic power [24]. Studies in humans [2], rats [11] and dogs [13] have shown that increasing the fat content of an isocaloric diet resulted in an increase in O2 max. This may be due to the higher oxygen cost of re-synthesizing ATP from fat and/or enhancement of fat oxidizing capacity [2,4,11,25,26]. It may be that increased oxidative capacity in muscle is due to increasing the mass of mitochondria [10], as seen in dogs fed a high fat diet [13].

The present study did not demonstrate an increased O2 max in either the female or male subjects. However, 12 of the 25 had an increase in their O2 max. The maximal heart rate, lactic acid and R values, which were not different among the diets, were consistent with the subjects’ achieving O2 max and are similar to those in a previous study [2]. This would indicate the validity of the O2 max data. The major difference between this and the preceding study from our laboratory is the characteristics of the subjects. While subjects in both studies trained a similar mileage per week, the intensity of the present study’s subjects’ training was significantly lower. In addition, the percent of body fat of both the males and females (which is expected) was significantly higher than in the males in the previous study [2].

A potential risk of increasing the fat content of the diet by reducing carbohydrate content is compromised muscle glycogen stores [5]. One way to determine if glycogen stores are depleted is to use an anaerobic performance test like the Wingate Anaerobic Power test. Although both aerobic and anaerobic pathways contribute to ATP resynthesis during the all-out cycle against a fixed resistance for 30 seconds of exercise [27], the oxidative contribution is very small. Therefore, the Wingate test is considered a good measure of anaerobic power [14]. There was no decrease in anaerobic power on the medium or high fat diet, implying that glycogen stores were not seriously depleted. Replacing carbohydrate with fat in a hypocaloric diet may reduce O2 max due to reduced muscle glycogen stores [5]. However, in the present study, the carbohydrate levels, which were similar in all diets due to an increase in caloric intake, appeared to be sufficient to maintain muscle glycogen stores.

Endurance:
Studies using untrained moderately trained or subjects on a hypocaloric diet suggest that endurance performance is compromised on a high-fat diet and improved on a high-carbohydrate diet [5,25,28]. Highly trained subjects have higher glycogen levels [29] and a higher potential for lipid utilization [30]. Intramuscular glycogen concentration is not a limiting factor in trained runners during a middle-distance exercise (75% to 85% of O2 max) [31]. Consequently, carbohydrate-loading diets may not always be advantageous to endurance trained athletes [31]. This has been demonstrated by previous studies in man [2], rat [11] and dog [13] and is confirmed in the present study for both female and male athletes.

The relative role of carbohydrate and fat stores during exercise is dependent upon substrate utilization and can be inferred from the R value (ratio of CO2 and O2). This increased from 0.84 to 0.94, going from 30% to 80% of O2 max on both the O2 max test and during the first phase of the endurance run. These values are consistent with those of previous studies [3,25,32]. During the second phase of the endurance run, the R did not change and was not affected by dietary fat intake. This observation is in disagreement with previous studies [25,33]. This apparent discrepancy may be due to the higher caloric intake in the present study; the higher carbohydrate and fat intake presumably increased muscle glycogen and triglyceride stores. It has been suggested that the intensity of the exercise is a more important determinant of the R than muscle or blood substrate concentrations [31]. Our data support this, as the R was not influenced by the carbohydrate or fat intake.

The R can be influenced by the respiratory compensation for metabolic acidosis. R may be overestimated when intensity is at or above 75% to 80% of O2 max due to CO2’s being artificially high. As the lactate levels were 3 to 4 fold above rest, it is reasonable to assume that the measured R is an overestimation of cellular CO2. If so, given an R of 0.94 during the endurance run at 80% of O2 max, fat oxidation is probably contributing more to energy production than has been previously thought. This observation supports previous studies at 60% and 70% of O2 max, where increasing the dietary fat intake resulted in an improved endurance time [2].

Substrate availability is a function of intramuscular stores and delivery from the blood. We did not directly measure carbohydrate stores, but at this exercise intensity carbohydrate metabolism should not limit the endurance run, as under similar conditions glycogen levels are not sufficiently depleted [34]. Consistent with this is the sustained increase in lactic acid during the run at 80% of O2 max. In addition, the lower lactate and higher pyruvate levels on the high fat diet suggest that the uptake of pyruvate was limited, despite the potential to increase O2. Nevertheless, the lactate levels at the end of the endurance run were much less than after the O2 max test, indicating lactate or pH were not limiting factors in the endurance run.

Considering the observed increase in blood glucose, it appears that glucose from the plasma does not play an important role in cellular metabolism at these high work rates [34]. In addition, at high intensity, there is a limited transport capacity for glucose from blood to muscle cells [5].

The release into and transport by the blood of fats to the muscle in response to exercise is represented by the levels of free fatty acids, triglycerides and glycerol. Free fatty acids and triglyceride levels were not affected by diet, while glycerol levels were significantly elevated after exercise. The elevated glycerol with increased exercise intensity is an indication of increased adipose or muscle tissue lipolysis. Since the intensity of the exercise was the same among the three diets, it is not surprising that lipolysis was similar. The observation that free fatty acid levels did not increase suggests that release was equivalent to uptake on each diet. The use of fat was not different, based on the similar R values. It has been reported that exercise-induced free fatty acid mobilization lags behind muscle uptake [34,35]; this may explain why the plasma levels remained constant in spite of the increased mobilization. The source of this lipolysis was not determined, but it is possible that on the high fat diet more was coming from the muscle stores and this would explain the lack of a high free fatty acid level in the plasma on the high fat diet.

Since a low fat diet may result in reduced availability and refilling of intramuscular fat stores [2,21,32,36], the observation that endurance improved on the higher fat diets may be the result of use or replenishment of diminished endogenous fat stores. This is consistent with other studies [2,37]. During exercise, at 75% to 85% of O2 max, mobilization and/or uptake of fat from adipose tissue may be limited and intramuscular fat stores becomes crucial. Numerous studies have reported that muscle triglyceride stores are depleted even during high intensity aerobic exercise [38,39,40]. Thus, low intramuscular fat may provide a limitation to exercise endurance. This may limit exercise endurance in highly trained runners [40]. This is consistent with what we observed in our runners on the low fat diet.

In a recent study, subjects who were trained on a high fat diet [41] failed to improve performance. However, the carbohydrate intake was less than in the present study due to the low total caloric intake.

The lack of significantly improved endurance exercise performance on the high fat diet suggests that either the medium fat, isocaloric diet keeps both muscle glycogen and fat stores filled or that the relative increase in fat intake from 33% to 44% was not of the same magnitude as from 16% to 31% and was therefore insufficient to increase muscle aerobic capacity. There were changes in metabolic balance during the endurance run on the high fat diet as the subjects’ lactic acid levels were lower and pyruvate levels were higher. This could relate to the fact that the runners used in the present study were not accustomed to running at 80% of O2 max during training and therefore stopped prematurely. This is difficult to reconcile as maximal heart rates and lactates were reached in all of the endurance profiles and there were no differences among the diets.


    CONCLUSIONS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
These data support previous studies demonstrating that increased dietary fat intake without compromising carbohydrate intake improves endurance performance. If the diet is hypocaloric, however, increasing fat and decreasing carbohydrates reduces glycogen stores and impairs performance. Clearly demonstrated by the reduced running capacity on the low fat diet, reduction in total calories and/or fat is not conducive to optimal exercise performance. It is suggested that the intramuscular stores of glycogen and fats are the crucial ones as the rate of supply from the blood is too slow to meet energy requirements. The blood substrates are important for the replenishment of intramuscular stores during recovery from exercise. The present study extends these observations to female runners and runners of a more recreational nature. The present study does not support the hypothesis that increasing fat to 44% of total calories improves performance to a greater extent than does 31% fat; however, further studies using more intensely trained athletes with lower body fat are needed.


    ACKNOWLEDGMENTS
 
This work was partially supported by a research grant from Mars, Inc. The authors would like to acknowledge the help of Hans Hoppler, Ph.D., Dick Taylor, Ph.D., Jaya Venkatraman, Ph.D., Stacie D. Ryer-Calvin, Charlotte Baumgardt, M.S., R.D., Juliet Gilbert, Kathryn Gutillo, Brian Jakubowicz, Melanie Rimmer, Jill Rowland, Kerry Sheeley and Mike Washo, R.D.

Received December 1, 1996. Revised November 1, 1996.
    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 

  1. Brozek J, Grande F, Anderson J, Keys A: Densitometric analysis of body composition: revision of some quantitative assumptions. Ann NY Acad Sci 110: 113–140, 1963.
  2. Muoio DM, Leddy JJ, Horvath PJ, Awad AB, Pendergast DR: Effect of dietary fat on metabolic adjustments to maximal O2 and endurance in runners. Med Sci Sports Exerc 26: 81–88, 1994.[Medline]
  3. Miller WC, Bryce GR, Conlee RK: Adaptations to a high-fat diet that increase exercise endurance in male rats. J Appl Physiol 56: 78–83, 1984.[Abstract/Free Full Text]
  4. Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL: The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 32: 769–776, 1983.[Medline]
  5. Costill DL: Carbohydrates for exercise: dietary demands for optimal performance. Intl J Sports Med 9: 1–18, 1988.[Medline]
  6. Bosch AN, Dennis SC, Noakes TD: Influence of carbohydrate loading on fuel substrate turnover and oxidation during prolonged exercise. J Appl Physiol 74: 1921–1927, 1993.[Abstract/Free Full Text]
  7. Thompson JL, Manore MM, Skinner JS, Ravussin E, Spraul M: Daily energy expenditure in male endurance athletes with differing energy intakes. Med Sci Sports Exerc 27: 347–354, 1995.[Medline]
  8. Almeras N, Lavallee N, Despres JP, Bouchard C, Tremblay A: Exercise and energy intake: effect of substrate oxidation. Physiol Behav 57: 995–1000, 1996.
  9. Tremblay A, Plourde G, Despres JP, Bouchard C: Impact of dietary fat content and fat oxidation on energy intake in humans. Am J Clin Nutr 49: 799–805, 1989.[Abstract/Free Full Text]
  10. Holloszy JO: Biochemical adaptations in muscle: effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. J Biol Chem 242: 2278–2282, 1967.[Abstract/Free Full Text]
  11. Simi B, Sempore B, Mayet MH, Favier RJ: Additive effects of training and high-fat diet on energy metabolism during exercise. J Appl Physiol 71: 197–203, 1991.[Abstract/Free Full Text]
  12. Carlson LA, Ekelund LG, Froberg SO: Concentration of triglycerides, phospholipids and glycogen in skeletal muscle and of free fatty acids and b-hydroxybutyric acid in blood in man in response to exercise. Eur J Clin Invest 1: 248–254, 1971.[Medline]
  13. Taylor CR, Hoppeler H, Kennedy C, Valenski T, Roberts TJ, Weyand P: High fat diet improves aerobic performance by building mitochondria. FASEB J 9: 11029, 1995.
  14. Dotan R, Bar-Or O: Load optimization for the Wingate Anaerobic Test. Eur J Appl Physiol 51: 409–417, 1983.
  15. Itaya K: A more sensitive and stable colorimetric determination of free fatty acids in blood. J Lipid Res 18: 663–665, 1977.[Abstract]
  16. Horswill CA, Hickner RC, Scott JR, Costill DL, Gould D: Weight loss, dietary carbohydrate modifications and high intensity, physical performance. Med Sci Sports Exerc 22: 470–476, 1990.[Medline]
  17. McMurray RG, Ben-Ezra V, Forsythe WA, Smith AT: Responses of endurance-trained subjects to caloric deficits induced by diet or exercise. Med Sci Sports Exerc 17: 574–579, 1985.[Medline]
  18. Despres JP, Bouchard C, Savard R, Tremblay A, Marcotte M, Theriault G: The effect of a 20-week endurance training program on adipose-tissue morphology and lipolysis in men and women. Metabolism 33: 235–239, 1984.[Medline]
  19. Sherman WM, Costill DL: The marathon: dietary manipulation to optimize performance. Am J Sports Med 12: 44–51, 1984.[Abstract/Free Full Text]
  20. Calles-Escandon J, Driscoll P: Free fatty acid metabolism in aerobically fit individuals. J Appl Physiol 77: 2374–2379, 1994.[Abstract/Free Full Text]
  21. Jacobs I, Lithell H, Karlsson J: Dietary effects on lipoprotein lipase activity in skeletal muscle in man. Acta Physiol Scand 115: 85–90, 1982.[Medline]
  22. Jansson E, Kaijser L: Substrate utilization and enzymes in skeletal muscle of extremely endurance-trained men. J Appl Physiol 62: 999–1005, 1987.[Abstract/Free Full Text]
  23. Brownwell KD, Nelson Steen S, Wilmore JH: Weight regulation practices in athletes: analysis of metabolic and health effects. Med Sci Sports Exerc 19: 546–556, 1987.[Medline]
  24. Green HJ, Patla AE: Maximal aerobic power: neuromuscular and metabolic considerations. Med Sci Sports Exerc 24: 38–46, 1992.[Medline]
  25. Bergstrom J, Hermansen L, Hultman E, Saltin B: Diet, muscle glycogen and physical performance. Acta Physiol Scand 71: 140–150, 1967.[Medline]
  26. Dyck DJ, Putman CT, Heigenhauser GJF, Hultman E, Spriet LL: Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling. Am J Physiol 265: E852–E859, 1993.[Abstract/Free Full Text]
  27. Granier P, Mercier B, Mercier J, Anselme F, Prefaut C: Aerobic and anaerobic contribution to Wingate test performance in sprint and middle-distance runners. Eur J Appl Physiol 70: 58–65, 1995.
  28. Karlsson J, Saltin B: Diet, muscle glycogen, and endurance performance. J Appl Physiol 31: 203–206, 1971.[Free Full Text]
  29. Piehl K, Adolfsson S, Nazar K: Glycogen storage and glycogen synthetase in trained and untrained muscle of man. Acta Physiol Scand 90: 779–788, 1974.[Medline]
  30. Karlsson J, Nordesjo L, Saltin B: Muscle glycogen utilization during exercise and physical training. Acta Physiol Scand 90: 210–217, 1974.[Medline]
  31. Madsen K, Pedersen PK, Rose P, Richter EA: Carbohydrate supercompensation and muscle glycogen utilization during exhaus-tive running in highly trained athletes. Eur J Appl Physiol 61: 467–472, 1990.
  32. Kiens B, Essen-Gustavsson B, Christensen NJ, Saltin B: Skeletal muscle substrate utilization during submaximal exercise in man: effect of endurance training. J Physiol 469: 459–478, 1993.[Abstract/Free Full Text]
  33. Jansson E: On the significance of the respiratory exchange ratio after different diets during exercise in man. Acta Physiol Scand 114: 103–110, 1982.[Medline]
  34. Marliss EB, Simantirakis E, Miles PDG, Hunt R, Gougeon R, Purdon C, Halter JB, Vranic M: Glucose turnover and its regulation during intense exercise and recovery in normal male subjects. Clin Invest Med 15: 406–419, 1992.[Medline]
  35. Gorski J: Muscle triglyceride metabolism during exercise. Can J Physiol Pharmacol 70: 123–131, 1992.[Medline]
  36. Moffatt RJ: Dietary status of elite female high school gymnasts: inadequacy of vitamin and mineral intake. J Amer Diet Assoc 84: 1361–1363, 1984.
  37. Soza M, Karpati G: Skeletal muscle endurance: the effect of increased availability of endogenous long-chain fatty acid fuel. Exp Neurol 91: 449–462, 1986.[Medline]
  38. Hurley BF, Nemeth PM, Martin WH III, Hagberg JM, Dalsky GP, Holloszy JO: Muscle triglyceride utilization during exercise: effect of training. J Appl Physiol 60: 562–567, 1986.[Abstract/Free Full Text]
  39. Jones NL, Heigenhauser JF, Kuksis A, Matsos CG, Sutton JR, Toews CJ: Fat metabolism in heavy exercise. Clin Sci 59: 469–478, 1980.[Medline]
  40. Staron RS, Hikida RS, Murray TF, Hagerman FC, Hagerman MT: Lipid depletion and repletion in skeletal muscle following a marathon. J Neurol Sci 94: 29–40, 1989.[Medline]
  41. Helge JW, Richter EA, Kiens B: Interaction of training and diet on metabolism and endurance during exercise in man. J Physiol 492: 293–306, 1996.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
Br. J. Sports. Med.Home page
J. Sundgot-Borgen and M. K. Torstveit
The female football player, disordered eating, menstrual function and bone health
Br. J. Sports Med., August 1, 2007; 41(suppl_1): i68 - i72.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
D. E. Larson-Meyer, B. R. Newcomer, and G. R. Hunter
Influence of endurance running and recovery diet on intramyocellular lipid content in women: a 1H NMR study
Am J Physiol Endocrinol Metab, January 1, 2002; 282(1): E95 - E106.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Coll. Nutr.Home page
J. T. Venkatraman, X. Feng, and D. Pendergast
Effects of Dietary Fat and Endurance Exercise on Plasma Cortisol, Prostaglandin E2, Interferon-{gamma} and Lipid Peroxides in Runners
J. Am. Coll. Nutr., October 1, 2001; 20(5): 529 - 536.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Horvath, P. J.
Right arrow Articles by Pendergast, D. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Horvath, P. J.
Right arrow Articles by Pendergast, D. R.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS