High-Fat Diet Versus Habitual Diet Prior

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High-Fat Diet versus Habitual Diet Prior to

Carbohydrate Loading: Effects on Exercise Metabolism
and Cycling Performance
Article in International Journal of Sport Nutrition and Exercise Metabolism · June 2001

DOI: 10.1123/ijsnem.11.2.209 · Source: PubMed
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High-Fat Diet and Exercise / 209
International Journal of Sport Nutrition and Exercise Metabolism, 2001, 11, 209-225
© 2001 Human Kinetics Publishers, Inc.
High-Fat Diet Versus Habitual Diet Prior

to Carbohydrate Loading: Effects on Exercise
Metabolism and Cycling Performance
Estelle V. Lambert, Julia H. Goedecke, Charl van Zyl,

Kim Murphy, John A. Hawley, Steven C. Dennis,
and Timothy D. Noakes
We examined the effects of a high-fat diet (HFD-CHO) versus a habitual diet,
prior to carbohydrate (CHO)-loading on fuel metabolism and cycling time-trial
(TT) performance. Five endurance-trained cyclists participated in two 14-day
randomized cross-over trials during which subjects consumed either a HFD
(>65% MJ from fat) or their habitual diet (CTL) (30 ± 5% MJ from fat) for 10
day, before ingesting a high-CHO diet (CHO-loading, CHO > 70% MJ) for 3
·
days. Trials consisted of a 150-min cycle at 70% of peak oxygen uptake (VO2peak),
followed immediately by a 20-km TT. One hour before each trial, cyclists ingested
400 ml of a 3.44% medium-chain triacylglycerol (MCT) solution, and during the
trial, ingested 600 ml/hour of a 10% 14C-glucose + 3.44% MCT solution. The
dietary treatments did not alter the subjectsʼ weight, body fat, or lipid profile.
There were also no changes in circulating glucose, lactate, free fatty acid (FFA),
and -hydroxybutyrate concentrations during exercise. However, mean serum
glycerol concentrations were significantly higher (p < .01) in the HFD-CHO
trial. The HFD-CHO diet increased total fat oxidation and reduced total CHO
oxidation but did not alter plasma glucose oxidation during exercise. By contrast,
the estimated rates of muscle glycogen and lactate oxidation were lower after the
HFD-CHO diet. The HFD-CHO treatment was also associated with improved
TT times (29.5 ± 2.9 min vs. 30.9 ± 3.4 min for HFD-CHO and CTL-CHO, p <
.05). High-fat feeding for 10 days prior to CHO-loading was associated with an
increased reliance on fat, a decreased reliance on muscle glycogen, and improved
time trial performance after prolonged exercise.
Key Words: high-fat diet, medium-chain triacylglycerols, muscle glycogen,

glucose metabolism, fat metabolism
The authors are with the Research Unit for Exercise Science and Sports Medicine in
the Department of Human Biology, Faculty of Health Sciences, University of Cape Town,
Sports Science Institute of South Africa, Newlands 7725, Cape Town, South Africa.
209
210 / Lambert et al.
Introduction
There is an ongoing debate regarding the impact of a fat-rich, low-carbohydrate
(CHO) diet on the regulation of substrate oxidation and exercise performance dur-
ing prolonged exercise at moderate to high intensities (11;15;18;19;25;28;30;31).
The debate is exacerbated by methodological differences, including the nature of
the exercise bout (duration and intensity), the measurement of exercise performance
(endurance capacity, the amount of work completed in a specified time, or a time trial)
and the definition of a fat-rich diet (% of energy and duration of intake). The effects
of a high-fat diet may be further confounded by the nutritional state of the subjects
prior to the trials (fed or fasted), the pre-exercise meal (the nutrient and energy com-
position) and the resultant hormonal milieu during the exercise bout.
Compared to a high-CHO diet, the consumption of a high-fat diet for 3–7 days
Downloaded by W VA Univ Library on 09/16/16, Volume 11, Article Number 2
has resulted in a decrease in submaximal exercise time to exhaustion (2, 5, 13, 21,
23, 27, 35). On the other hand, there is evidence that the ingestion of a fat-rich diet
for longer periods (≥7 days) induces adaptive responses that are fundamentally dif-
ferent to the acute lowering of body CHO reserves or fasting (4, 11, 15, 18, 19, 30,
32). Studies examining the effects of more prolonged high-fat feeding (≥2 weeks)
have shown an increase in carnitine-acyl transferase activity (11, 15), a decrease in
hexokinase activity (11), a decrease in insulin-stimulated muscle glucose uptake (24,
32), a decreased oxidative glucose disposal by the muscle, and a reduction in skeletal
muscle pyruvate dehydrogenase activity in exercise-trained humans (9).
Possibly due to these adaptations, exposure to a fat-rich, low-CHO diet for 1–5
weeks in well-trained individuals has been shown to maintain (15, 19, 30, 31) and
even enhance (25) endurance capacity during exercise of low to moderate intensities.
Furthermore, fat-rich diets are associated with decreased CHO oxidation during
exercise, decreased reliance on muscle and liver glycogen stores, and increased
glycogen synthase activity (9).
Conlee et al. (7) have shown that rats adapted to a high-fat diet for 4–5 weeks
and subsequently fed a high-CHO diet for 3 days, rapidly repleted muscle glyco-
gen stores to pre-diet levels and ran longer during constant-load treadmill exercise
than the CHO-adapted rats. Conversely, Helge et al. (18) fed untrained young male
subjects a high–fat diet or a high-CHO diet for a period of 7 weeks, followed by 1
week of CHO-loading, showed similar rates of fat oxidation and muscle glycogen
depletion during exercise under the two conditions. Moreover, exposure to the high-
fat diet impaired endurance performance during a steady-state cycle to exhaustion.
Helge et al. (18) suggested that prolonged (7 week) high-fat feeding might alter the
membrane phospholipid composition and change calcium transport in the cytoplasm,
compromising endurance performance.
It was, therefore, hypothesized that adaptation to a high-fat diet for a period
sufficient to elicit metabolic adaptations in favor of fat oxidation, followed by short-
term exposure to a high-CHO diet, would enhance fat oxidative capacity and “spare”
muscle glycogen stores, with the potential for optimizing exercise performance.
Therefore, the aims of the present investigation were (a) to study the effects of
a 10-day high-fat, low-CHO diet, followed by 3 days of CHO-loading, on substrate
utilization during constant-load, submaximal exercise; and (b) to determine the ef-
fects of such a diet on subsequent high-intensity cycling performance.
Table 1 Subject Characteristics
Variable Mean ± SEM
Age (years) 22.4 ± 1.5

Height (m) 1.80 ± 0.02
Mass (kg) 77.4 ± 1.8
Body fat (%) 13.7 ± 1.4
PPO (W) 393.5 ± 18.1
·
VO2peak (L · min–1) 4.9 ± 0.2
·
Note. PPO = peak power output; VO2peak = peak oxygen con-
sumption.
Materials and Methods

Subjects
Five male endurance-trained cyclists participated in this study, which was approved
by the Research and Ethics Committee of the Faculty of Medicine of the University
of Cape Town. Because trace amounts of [U-14C] glucose were ingested and venous
blood samples were taken, the risks were carefully explained to each subject before
their written consent was obtained. All subjects were healthy, had been cycling on
a regular basis for more than 3 years, and consumed habitual diets that contained
less than 40% of total energy intake from fat. The characteristics of the subjects are
presented in Table 1.
Preliminary Testing
All subjects were tested for peak oxygen consumption (V·O2peak) and peak sustained
power output (PPO) on an electronically braked cycle ergometer (Lode, Groningen,
Holland) modified with clip-in pedals or toe clips and racing handle bars. The incre-
mental cycle test to exhaustion, the determination of PPO, and the accompanying
gas collection procedures have been described in detail previously (17). Briefly,
each subject began cycling at a workload of 3.33 W · kg–1 · min–1 body mass for 150
s. This workload was then increased by 50 W for a further 150 s and, thereafter, the
exercise intensity was increased by 25 W for 150 s until the subject was exhausted.
Exhaustion was defined as a reduction in pedaling frequency of > 10 rpm and/or a
respiratory exchange ratio (RER) > 1.10. PPO was defined as the last completed work
rate plus the fraction of time spent in the final non-completed work rate multiplied
by the 25 W work rate increase.
During the progressive exercise test, subjects wore a nose-clip and inspired
air via a Hans Rudolph 2700 one-way valve (Vacumed, Ventura, CA) connected to
a dry gas meter. The expired air was passed though a 15-L baffled mixing chamber
and a condensation coil to an Ametek S-3A/I O2 analyzer and a CD-3A CO2 analyzer
(Scientific Instruments, Pittsburgh, PA). Before each test, the gas meters were cali-
brated with a Hans Rudolph 5530 3-L syringe, room air, and a 16% CO2 : 4% O2 :
80% N2 gas mixture. The instrument outputs were processed by an on-line computer
that calculated L · min–1 in ventilation (V·E), V·O2, and expired CO2 (V·CO2) values
using conventional equations. The results of the initial maximal test were used to
determine the workload, which corresponded to ~63% of each subjectʼs PPO (~70%
of V·O2peak), for the subsequently described experimental trials.
Dietary Manipulations
The subjectsʼ habitual dietary intake was assessed using a 3-day weighed dietary
record, consisting of 2 week days and 1 weekend day. The diets were analyzed us-
ing the Food Finder program (Medtech Ltd., Medical Research Council, Tygerberg,
South Africa) to determine energy intake and macronutrient composition (Table 2).
From the analysis of each subjectʼs habitual diet, isoenergetic high fat (HFD) and high
CHO diets were formulated for each subject (Table 2). Prior to each experimental
trial, subjects underwent two randomly assigned, 10-day periods of either HFD
(>65% energy from fat) followed by 3 days of a high-CHO diet (>65% energy from
CHO)(HFD-CHO), or 10 days of their habitual diet (CTL), followed by 3 days of a
high-CHO diet (CTL-CHO). To aid compliance to the diets, palatable, individualized
menus were formulated for each subject by a registered dietician. All food was
purchased for the subjects; however, subjects were free-living and were instructed
to follow the diets to the best of their ability. A sample high fat menu, including the
energy intake and macronutrient composition, is provided in Table 3.
The prescribed diets aimed at providing an isocaloric intake compared with
the habitual diet, with similar protein intakes (20% by energy). There were no re-
ported deviations from the prescribed diets and purchased food items. However, if
subjects did not adhere strictly to the diets, then the effects may have actually been
underestimated. Compliance was indirectly confirmed by the high initial rates of
total fat oxidation after exposure to the high-fat diet.
Experimental Trial
Prior to the first trial, subjects underwent a familiarization ride in order to minimize
any possible learning effect of the trial. Trials were separated by a 2-week period,
during which time the subjects continued with their normal training and reverted
Table 2 Nutrient Composition (by Energy) of the Dietary Interventions
Variable Habitual diet High-fat diet High-CHO diet
Energy (MJ) 14.3 ± 0.7 14.00 14.00

CHO (%) 52.6 ± 5.8 <15% >65%
Fat (%) 29.9 ± 4.5 >65% <15%
Protein (%) 12.8 ± 0.9 20% 20%
Alcohol (%) 2.1 ± 1.1 — —
Note. Values are mean ± SEM.

Table 3 Sample Menu of a High-Fat Diet
Breakast: 60 g fried South African sausage (boerewors)

70 g avocado
50 g fried tomato
50 g fried onion
Snack: 50 g peanuts
Lunch: 100 g green salad
23 g mayonnaise
90 g tuna in oil
50 g cheese
50 g bread roll
10 g margarine
10 g peanut butter
Snack: 30 g crisps
Dinner: 100 g green salad
23 g salad dressing
120 g fried pork sausage
100 g fried potatoes
50 g fried onions
Snack: 50 g peanuts
20 g cream to be added to 2 cups of coffee
Nutrient content: Energy (MJ) 13.5
CHO (%) 13.5
Fat (%) 71.1
Protein (%) 13.9
back to the consumption of their habitual diets. Subjects were asked to refrain from
riding on the day preceding the experimental trial.
Each trial consisted of a 150-min cycle at 63% of PPO (~70% of V·O2peak) on
the electronically-braked ergometer, followed immediately by a simulated 20-km
time-trial (TT). The 20-km TT was performed on the subjectʼs own bicycle mounted
on a Kingcycle Trainer (EDS Portaprompt, Ltd., UK). The calibration and reliability
of the Kingcycle has been described in detail previously (29). The coefficient of
variation for 6 subjects who undertook three 20-km TT was 1.1 ± 0.9%. Throughout
each experimental trial, power output and cadence were monitored every 60 s, but
the only feedback given to subjects was their elapsed distance (as a percentage of
the total distance). Subjects were cooled with an electronic fan, and the laboratory
was maintained at a constant temperature of 20 °C and approximately 55% relative
humidity.
Experimental trials were conducted between 0700–1100 hours. Upon arrival
at the laboratory, each subjectʼs height and body mass were recorded, and percentage
body fat was estimated using the sum of four skinfolds (10). Thereafter, a flexible
18-gauge cannula (Johnson and Johnson, Halfway House, South Africa) was attached
to a 3-way stop-cock (Industries Palex Plc, Barcelona, Spain) and positioned in a

forearm antecubital vein for the collection of blood samples at rest and at 20-min
intervals throughout each trial. After a blood sample was taken, the cannula was im-
mediately flushed with 2–3 ml of sterile saline plus 5 L of heparin.
One hour before the start of both trials, subjects consumed 400 ml of a 3.44%
(g · 100–1 ml) MCT (C8–10): 0.86% long-chain triacylglycerol (LCT) solution (Lip-
rocil, Adcock Ingram, Critical Care Ltd., Johannesburg, South Africa). After 60 min,
subjects mounted the cycle ergometer and began a 5-min warm-up at a workload of
100 W. The constant-load ride at 63% of PPO was then commenced, with subjects
ingesting 100 ml of a combined 10% glucose polymer + 3.44% MCT solution every
10 min until completion of the trial. The MCT and CHO solution was given to subjects
in order to maximize potential fat and CHO oxidation during exercise (22, 38). All
drinks were flavored with a low calorie orange concentrate and labeled with trace
amounts of [U-14C] glucose (Amersham International, Buckinghamshire, UK) so

that rates of plasma and ingested glucose oxidation could be calculated from drink
and plasma 14C-glucose specific activities and expired 14CO2 specific activity.
· , VCO
VO · , and 14CO2 Measurements
2 2
Steady-state gas exchange was measured for 3–4 min every 20 min until the com-
pletion of the ride. Expired 14CO2 was trapped by passing air from the CO2 gas analyzer
vent through a solution containing 1 ml of 1 N hyamine hydroxide in methanol (United
Technologies, Packard, IL), 1 ml of 96% ethanol (SAARCHEM, Krugersdorp, RSA),
and 1–2 drops of phenolphthalein (SAARCHEM). The expired air was bubbled
through the trapping mixture until the solution became clear, at which point 1 mmol
of CO2 had been absorbed (33). Liquid scintillation cocktail (Ready Gel, Beckman,
Fullerton, CA) was then added, and 14CO2 radioactivity was counted in a liquid
scintillation counter (Packard Tri-Carb 1500, Downers Grove, IL). All counts were
corrected for differences in quench and background disintegrationʼs min–1 (dpm).
Blood Sampling and Analysis

Blood samples (~12 ml) were collected at rest, and then after 40, 80, 100, 120, 140
min during the steady-state ride; at 160 min; and within 1 min of completing the
TT. One aliquot (5 ml) was placed into a tube containing potassium oxalate and
sodium fluoride for the subsequent analyses of plasma glucose, lactate, and plasma
14
C-glucose concentrations. Another aliquot (3 ml) was placed in a tube containing
lithium heparin for the subsequent analysis of plasma insulin concentrations. The
remaining aliquot (3 ml) was placed in a tube containing gel and clot activator for
determinations of serum free (non-esterified) fatty acids (FFA), glycerol and -hy-
droxybutyrate concentrations. All samples were kept on ice, centrifuged at 3,000
rpm at 4 °C for 10 min at the end of the trial, and supernatants were then stored at
–20 °C for later analyses.
Plasma glucose concentrations were determined in duplicate using an auto-
mated glucose analyzer (Glucose Analyser II, Beckman Instruments, Fullerton, CA),
while plasma insulin concentrations were measured by radio-immunoassay (Count-
A-Coat Insulin, Diagnostic Products, Los Angeles, CA). Plasma lactate concentra-
tions (Bio Merieux, Marcy-L Etiole, France) and total plasma FFA concentration
(Half-micro test, Boehringer Mannheim, Germany) were determined by enzymatic
spectrophotometric assays. Serum glycerol and - hydroxybutyrate were measured

enzymatically according to the methods of Bergmeyer (1).
On days 0, 5, and 10 of the HFD-CHO, a 5-ml blood sample was drawn from
each subject and placed in a tube containing EDTA for the subsequent enzymatic
analysis of serum cholesterol (Boehringer Manneheim, Germany). HDL cholesterol
concentrations were determined after selective precipitation of the apoB-containing
lipoproteins with manganese chloride and heparin (14).
Plasma Glucose and Lactate Specific Activity

A 1-ml aliquot of the plasma, which was collected during the steady-state ride, was
added to a tube containing 70 L of 50% PCA for the separation of glucose and
lactate. After the sample was mixed, and centrifuged at 5,000 rpm for 10 min at 4
°C, the protein-free supernatant was removed and stored at 3 °C. The precipitate
was then re-suspended in 0.78 ml of 1.9% PCA and re-centrifuged at 5,000 rpm for
10 min at 4 °C, and the supernatant was added to that previously saved. This step
was repeated before the pellet was discarded, and the combined supernatants were
adjusted to pH 7–8 with ~200 L of MK2CO3 (3 mol · L–1), made in 0.01 M TRIS-
HCl buffer (pH 8.0). The solution was then centrifuged at 5,000 rpm for 20 min at
4 °C. The supernatant was subsequently passed through anion exchange columns
containing Sephadex (Bakerbond SAX, Cape Town, South Africa) that had been
conditioned with 20 ml of ethanol followed by 20 ml of distilled water adjusted to
pH ~8 with trace amounts of NaOH. Glucose was fully eluted into a scintillation
vial with 3  1 ml of distilled water (pH ~8). Lactate was subsequently eluted into a
second scintillation vial with 2  1 ml of CaCl2 (1 mol · L–1), adjusted to pH ~2 with
HCl. After collection, the eluates were evaporated to near dryness at 70 °C for ~20
hours before liquid scintillation cocktail (Ready Gel, Beckman, Fullerton, CA) was
added for 14C-counting as described earlier.
Each time glucose and lactate samples were separated, a non-labeled plasma
sample was spiked with a known quantity of [U-14C] glucose and run simultaneously
to correct the measured dpm values for the percent recovery. Such recoveries exceeded
90% for all samples. Since there were negligible counts in the lactate fraction, no
corrections were made for the contribution to V14CO2 from 14C-lactate oxidation.
Glucose Oxidation
The rates of plasma glucose oxidation (Gluox) in grams per minute were determined
from the equation:
GLU = (SA CO / SA glu) · V·CO

ox 2 2
In this equation, GLUox is the rate of plasma glucose oxidation in mmol · min–1. SA
CO2 is the specific (radio) activity of expired 14CO2 in dpm · mmol–1. SA glu is the
corresponding specific (radio) activity of the plasma glucose in dpm · mmol–1. V·CO2
is the volume of expired CO2 in mmol · min–1, calculated from the L · min–1 V·CO2 and
the 22.4 ml · mmol–1 gas volume. Since the complete conversion of one molecule of
U-14C glucose to six molecules of 14CO2 decreases the dpm · mmol–1 specific radioac-
tivity by a factor of six, the V·CO2 values did not need to be divided by six to allow for
six CO2 molecules arising from oxidation of one glucose molecule.
The same equation was used to determine the rates of ingested CHO oxidation.
However, in this case, SA glu was the specific radioactivity of the drink in dpm · mmol–1
glucose equivalents. It should be noted that this formula does not take into account
the time taken to equilibrate 14CO2 with the HCO3 pool, which has been reported to
vary between 5 min (8) and 90 min (6). However, it can be predicted from the flux
of CO2 through the body HCO3 stores that equilibration is essentially complete in
20–30 min (3). More to the point, any systematic lag in the appearance of 14CO2 in
the breath would have been similar from trial to trial.
Total CHO and Fat Oxidation

The overall rates of CHO and fat oxidation (grams per minute) were calculated from
the formulae of Frayn (12), assuming a non-protein RER. Differences between the
g/min rates of total CHO oxidation and plasma glucose oxidation provided an estimate
of the direct and/or indirect (via lactate) oxidation of muscle glycogen.
Statistical Analyses
All data are expressed as means ± SEM. We estimated that the minimal sample size
required to detect mean differences in fat oxidation during exercise between dif-
ferent dietary regimens of 0.30 g/min (with a standard deviation of 0.15 g/min) was
5 persons per group (or treatment) at an alpha level of .05, with 80% power. Factorial
analysis of variance was used to compare differences between treatments over time.
The Greenhouse-Geisser adjustment was used to correct for the maximal violation
of the assumption of sphericity in this repeated measures study design (39). Where
significant F-ratios were found, least squares post hoc analysis was performed to
determine differences at specific time points. An alpha level of p < .05 was considered
to be statistically significant. TT performance was compared using a paired t test
with two-tailed p values.
Results
Body Composition and Blood Lipid Profiles
Exposure to the HFD-CHO or the CTL-CHO diets did not alter body mass or esti-
mated body composition (Table 4). Nor were there any systematic changes in plasma
cholesterol or triacylglyerol concentrations in response to either dietary intervention
(Table 5).
Table 4 Variations in Body Composition With the CTL-CHO and HFD-CHO

Trials
Variable Pre CTL-CHO HFD-CHO
Weight (kg) 77.5 ± 1.8 78.2 ± 2.0 77.5 ± 2.1

Body fat (%) 13.7 ± 1.4 14.3 ± 1.6 13.5 ± 1.5
Note. Values are mean ± SEM. PRE = pre-trial values.

Table 5 Variations in Lipid Profile With the CTL-CHO and HFD-CHO Trials
Trial Day 5 Day 10 Day 13
Serum cholesterol (mmol · L–1):

PRE: 3.7 ± 0.3
CTL-CHO 3.36 ± 0.32 3.38 ± 0.33 3.31 ± 0.34
HFD-CHO 3.78 ± 0.39 3.69 ± 0.38 3.04 ± 0.42
Serum HDL-cholesterol
(mmol · L–1): PRE: 1.33 ± 0.08
CTL-CHO 1.25 ± 0.03 1.25 ± 0.04 1.10 ± 0.05
HFD-CHO 1.43 ± 0.07 1.38 ± 0.08 1.16 ± 0.09
Serum triglyceride (mmol · L–1):
PRE: 1.3 ± 0.2

CTL-CHO 1.21 ± 0.25 1.44 ± 0.22 1.07 ± 0.32
HFD-CHO 1.10 ± 0.23 1.16 ± 0.27 1.07 ± 0.17
Note. Values are mean ± SEM. HDL-cholesterol = high-density lipoprotein cholesterol;

PRE = pre-trial blood sample.
Serum-Free Fatty Acids (FFA), Glycerol, and -Hydroxybutyrate

Figure 1 displays the effects of the two dietary manipulations on the products of
triacylglycerol metabolism during the constant-load cycle and subsequent 20-km
TT. Mean serum glycerol concentrations were significantly higher in the HFD-CHO
trial compared to the CTL-CHO trial (p < .05). However, there were no differences
between dietary treatments for serum FFA or -hydroxybutyrate concentrations.
Serum FFA concentrations rose in both trials from 0.15–0.25 mmol · L–1 at the start
of exercise to ~0.45 mmol · L–1 at the end of the TT, which were significantly different
from resting after 120 min of steady-state exercise (p < .01).
Plasma Glucose, Blood Lactate, and Insulin Concentrations

The different dietary treatments also did not affect the plasma glucose and lactate
concentrations during the constant-load ride and TT. During both rides euglycaemia
was maintained, with an average plasma glucose concentration of between 4.5–5.5
mmol · L–1 (Figure 2). In both trials, mean plasma lactate concentrations rose from ~2
mmol · L–1 during the constant-load ride to ~4 mmol · L–1 at the end of the TT (Figure
2; p < .07). However, this response was variable between individuals.
Although plasma insulin concentrations during the constant-load ride tended
to be slightly higher following HFD-CHO diet, this difference did not reach statis-
tical significance (Figure 2). However, the area under the insulin curve (AUC) was
significantly greater following the HFD-CHO compared to the CTL-CHO trial (779 ±
129 mU · L–1 vs. 682 ± 129 mU · L–1 AUC, p < .001).
Total CHO, Plasma Glucose, Muscle Glycogen,

and Total Fat Oxidation Rates
Figure 1 — Serum free fatty acid (FFA), glycerol, and -hydroxybutyrate concentrations
during constant-load exercise and subsequent 20-km time trial. Serum FFA concen-
trations rose significantly in both trials and were significantly higher than resting values
after 120 min (p < .01). Mean serum glycerol concentrations were significantly higher in
the HFD-CHO trial than in the CTL-CHO trial (p < .05).
Total rates of CHO oxidation during exercise were significantly lower (p < .01) and
total fat oxidation was significantly higher (p < .05) in the HFD-CHO versus the
CTL-CHO trials. The average rates of CHO-oxidation in the CTL-CHO trial were
~1.7 g · min–1 compared to ~1.1 g · min–1 in the HFD-CHO trial.
In both trials, plasma glucose oxidation rose from ~0.35 g · min–1 after 60
min to ~0.8 g · min–1 at the end of the TT (Figure 4). Differences between rates of
total CHO oxidation and rates of plasma glucose oxidation suggested that the direct
and/or indirect (via lactate) oxidation of muscle glycogen were significantly greater
throughout the CTL-CHO trial compared to the HFD-CHO trial (Figure 4; p < .05).
The average calculated rates of direct and/or indirect (via lactate) muscle glycogen
oxidation were 1.08 ± 0.06 g · min–1 in the CTL-CHO trial and 0.63 ± 0.06 g · min–1
in the HFD-CHO trial.
Figure 2 — Plasma glucose, insulin, and lactate concentrations during constant-load

exercise and subsequent 20-km time trial. Plasma glucose levels were similar between
trials, and euglycaemia was maintained. Plasma lactate increase in both trials during
the time trial (p = .07). Plasma insulin decreased significantly in both trials after 60 min
of steady-state exercise (p < .01).
Cycling Time Trial Performances

Individual TT performances for the CTL-CHO and HFD-CHO trials are presented
in Figure 5. Time to complete the 20-km TT, following 2.5 hours of constant-load
exercise, were significantly shorter in the HFD-CHO trials compared to the CTL-CHO
trial (29.35 ± 1.25 min vs. 30.68 ± 1.55 min; p < .05). Improved TT performances
in the HFD-CHO trial were not associated with differences in either the subjective
ratings of perceived exertion or heart rates measured during the two trials.
Discussion
Figure 3 — Total CHO and fat oxidation during constant-load exercise and subsequent
20-km time trial. The rate of total CHO oxidation was significantly lower (p < .01), and
the rate of total fat oxidation was significantly higher (p < .05) in the HFD-CHO versus
CTL-CHO trials. Differences in substrate oxidation over time were not statistically
significant.
In the present study, 10 days of dietary fat-adaptation followed by a 3-day CHO-load-

ing regimen improved 20-km cycling TT performance, which was preceded by 150
min of constant-load exercise. In addition, we specifically fed subjects an MCT-CHO
suspension during exercise, as a readily oxidizable source of fat, used in this study
to maximize the rates of fat oxidation (38). The enhanced performance under the
HFD conditions in the present study was associated with a reduction in the estimated
rates of muscle glycogen utilization after the HFD compared to the habitual diet. To
the best of our knowledge, this is the first study that has specifically examined the
effect of a prolonged (>7 days) fat-adaptation regime followed by CHO-loading in
already well-trained subjects.
The only other study to examine the effects of a prolonged (7-week) period
of fat-adaptation followed by CHO-loading (1 week) was performed on previously
untrained subjects who undertook a 7-week endurance training program, followed
by 1 week of a high CHO diet (18). This rigorously controlled study showed that
prolonged exposure to a HFD attenuated some of the training-induced adaptations
normally associated with endurance exercise in subjects consuming a mixed diet.
This is despite the finding that there were similar rates of muscle glycogen depletion
during a submaximal ride to exhaustion after the two different dietary regimens.
Helge et al. (18) suggested that the earlier onset of fatigue following the high-fat
Figure 4 — Rates of plasma glucose oxidation and direct and/or indirect (via lactate)
oxidation of muscle glycogen during constant-load exercise and subsequent 20-km time
trial. Direct and/or indirect (via lactate) oxidation of muscle glycogen during exercise was
significantly lower in the HFD-CHO trial compared to the CTL-CHO trial (p < .05).
diet may be linked to changes in muscle membrane phospholipid composition and

to changes in calcium transport in the cytoplasm.
In the present study, CHO loading after the HFD effectively prevented the ex-
pected increase in serum FFA concentrations normally found in studies with high-fat,
low-CHO diets (21, 27, 30, 37). Therefore, differences in CHO oxidation between
trials cannot be explained on the basis of increased FFA availability. However, the
HFD-CHO diet may have resulted in an increased utilization of muscle triacylglyc-
erol, as evidenced by increased serum glycerol concentrations. Previous studies in
humans have shown an increase in intramuscular triacylglycerol stores following
both short-term [5 days, (21)] and long term [>2 weeks, (19)] consumption of a HFD.
Furthermore, Conlee et al. (7) have shown both increased storage and utilization of
intramuscular triacylglycerol during exercise in rats following 3–4 weeks of a HFD.
This adaptation, where overall fat oxidation is increased due to increased muscle
triacylglycerol oxidation, is similar to that seen with adaptation to endurance train-
ing (20, 26).
Differences in exercise performance and intermediary metabolism between the
present study and previous studies using short-term “glycogen-depletion” regimens,
combining several days of a high-fat diet with exhaustive exercise (2, 5, 13, 23, 27,
35), may be attributable, in part, to the metabolic sequelae in response to high fat
feeding. Short-term exposure to a high-fat diet (<7 days) results in impaired glucose
Figure 5 — 20-km time trial cycling performance following HFD-CHO and CTL-CHO
dietary interventions. Time to complete a 20-km time trial was significantly shorter after
the HFD-CHO diet compared to the CTL-CHO diet (p < .05).
tolerance (37), insulin resistance in the liver, and consequent decreased liver gly-
cogen synthesis (24). More recently, Schrauwen et al. (34) have demonstrated that
short-term exposure to a high-fat diet increases the oxidation of plasma triglyceride
derived fatty acid metabolism.
More prolonged high-fat feeding (≥2 weeks), however, has been shown to
increase carnitine-acyl transferase (11, 15) and decrease hexokinase (11) activities.
These changes are accompanied by a decrease in insulin-stimulated muscle glucose
uptake (24, 32) decreased oxidative glucose disposal by the muscle and a fall in
skeletal muscle pyruvate dehydrogenase activity in exercise-trained humans (9).
Although the effects of HFDs on insulin sensitivity and glucose metabolism in
rats have been shown to be partially and rapidly reversed by reducing the fat content
of the diet for 3 days (16), we found that the area under the insulin curve during 180
min of exercise was significantly higher after the HFD-CHO trial, despite the 3 days
of CHO-loading. These results suggest that there was some residual effect of the HFD
on insulin sensitivity, which might partially explain the attenuation of endogenous
CHO oxidation. The fact that there were no differences in the rates of plasma glucose
oxidation between HFD-CHO and CTL-CHO trials provides support that the site of
reduced insulin sensitivity in this study was in the muscle and not the liver. Failure
to show differences in blood glucose oxidation in the present study contrasts with
the findings of Phinney et al. (30). They showed that blood glucose oxidation was
three-fold lower after 4 weeks of a ketogenic diet. Such differences may be due to
either the CHO-loading regime undertaken by the subjects in the current study or
the ingestion of CHO during exercise.
Furthermore, in exercise-trained subjects, 3 weeks of dietary fat adaptation
has been shown to enhance insulin-stimulated, non-oxidative glucose disposal at
rest, and increase glycogen synthase activity (9). Sherman et al. (35) demonstrated
that CHO-loading following a period of CHO-depletion actually enhanced gly-
cogen storage capacity in the skeletal muscle. Although not measured in this study,
it is possible that the starting muscle glycogen concentrations were higher after the
HFD-CHO than the CTL-CHO dietary regimen, and that this was associated with
improved time trial performance.
One of the cautions often raised when studies of the effect of high-fat feeding
are undertaken is that this type of dietary regimen is potentially atherogenic (36).
However, in the present study, we found no systematic effect of high-fat feeding for
10 days on serum total cholesterol, HDL-cholesterol and triacylglycerol concen-
trations. Furthermore, we cannot exclude the role of possible motivational factors
associated with the diets on exercise performance, despite efforts to introduce the
feeding regimes to subjects in a way that would not favor one diet over the other.
All future studies of this nature should employ covert manipulation of the nutrient
content of the diet to minimize this possible source of bias.
In summary, the results of this study suggest that dietary fat adaptation (10 days,
fat > 65% by energy) followed by CHO-loading (3 days, CHO > 65% by energy) is
associated with improved cycle time trial performance after prolonged constant-load
exercise. These data provide some evidence that “nutritional periodization” may be
a useful strategy for prolonged endurance performance, and that high-fat feeding
prior to CHO loading may result in persistent adaptations favoring fat oxidation and
sparing of endogenous CHO, even during high-intensity exercise.
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Acknowledgments
We are grateful to Pharmacia, Inc. for providing the medium-chain triacylglycerol
gratis, and to Gary Wilson and Judy Belonje for their expert technical assistance. This
study was supported by the Medical Research Council of South Africa, and the Nellie
Atkinson and Harry Crossley Research Funds of the University of Cape Town.
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Article in International Journal of Sport Nutrition and Exercise Metabolism · June 2001

Estelle Victoria Lambert Julia Goedecke

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John A Hawley Timothy D Noakes

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High-Fat Diet Versus Habitual Diet Prior

Estelle V. Lambert, Julia H. Goedecke, Charl van Zyl,

Key Words: high-fat diet, medium-chain triacylglycerols, muscle glycogen,

Table 1 Subject Characteristics

Variable Mean ± SEM

Age (years) 22.4 ± 1.5

Materials and Methods

Table 2 Nutrient Composition (by Energy) of the Dietary Interventions

Variable Habitual diet High-fat diet High-CHO diet

Energy (MJ) 14.3 ± 0.7 14.00 14.00

Note. Values are mean ± SEM.

Table 3 Sample Menu of a High-Fat Diet

Breakast: 60 g fried South African sausage (boerewors)

to a 3-way stop-cock (Industries Palex Plc, Barcelona, Spain) and positioned in a

amounts of [U-14C] glucose (Amersham International, Buckinghamshire, UK) so

Blood Sampling and Analysis

spectrophotometric assays. Serum glycerol and - hydroxybutyrate were measured

Plasma Glucose and Lactate Specific Activity

GLU = (SA CO / SA glu) · V·CO

Total CHO and Fat Oxidation

Table 4 Variations in Body Composition With the CTL-CHO and HFD-CHO

Variable Pre CTL-CHO HFD-CHO

Weight (kg) 77.5 ± 1.8 78.2 ± 2.0 77.5 ± 2.1

Note. Values are mean ± SEM. PRE = pre-trial values.

Trial Day 5 Day 10 Day 13

Serum cholesterol (mmol · L–1):

PRE: 1.3 ± 0.2

Note. Values are mean ± SEM. HDL-cholesterol = high-density lipoprotein cholesterol;

Serum-Free Fatty Acids (FFA), Glycerol, and -Hydroxybutyrate

Plasma Glucose, Blood Lactate, and Insulin Concentrations

Total CHO, Plasma Glucose, Muscle Glycogen,

Figure 2 — Plasma glucose, insulin, and lactate concentrations during constant-load

Cycling Time Trial Performances

In the present study, 10 days of dietary fat-adaptation followed by a 3-day CHO-load-

diet may be linked to changes in muscle membrane phospholipid composition and

Human Kinetics, 1983, pp. 497-501.

triglyceride-derived fatty acid oxidation. Diabetes 49:640-646, 2000.

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