|
|
||||||||
Original Research |
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 |
|---|
|
|
|---|
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 |
|---|
|
|
|---|
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 |
|---|
|
|
|---|
|
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 subjects 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 |
|---|
|
|
|---|
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).
|
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.
|
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.
|
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%).
|
| DISCUSSION |
|---|
|
|
|---|
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 studys 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
CO2s 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 |
|---|
|
|
|---|
| ACKNOWLEDGMENTS |
|---|
Received December 1, 1996.
Revised November 1, 1996.
| REFERENCES |
|---|
|
|
|---|
O2 and endurance in runners.
Med Sci Sports Exerc
26:
8188,
1994.[Medline]
This article has been cited by other articles:
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |