Acute High-Intensity Interval Cycling Improves

Postprandial Lipid Metabolism

CHIA-LUN LEE1, YU-HSUAN KUO2, and CHING-FENG CHENG3
1
Division of Physical and Health Education, Center for General Education, National Sun Yat-Sen University, Kaohsiung,
TAIWAN; 2Department of Physical Education, National Taiwan Normal University, Taipei, TAIWAN; and 3Department of
Athletic Performance, National Taiwan Normal University, Taipei, TAIWAN

ABSTRACT
LEE, C.-L., Y.-H. KUO, and C.-F. CHENG. Acute High-Intensity Interval Cycling Improves Postprandial Lipid Metabolism. Med. Sci.
Downloaded from http://journals.lww.com/acsm-msse by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdtwnfKZBYtws= on 01/12/2021

Sports Exerc., Vol. 50, No. 8, pp. 1687–1696, 2018. Purpose: This study aimed to examine the effects of two exercise regimes on physio-
logical and postprandial lipemic responses. Methods: Thirty-six active men (peak oxygen uptake [V̇O2peak], 46.5 T 6.4 mLIkgj1Iminj1)
were randomly assigned to a high-intensity interval exercise (HIIE), involving 10  60 s cycling at 85% V̇O2peak interspersed with 120 s
recovery; a moderate-intensity continuous exercise (MICE), involving 50 min continuous exercise at 65% V̇O2peak; and a nonexercise
control (Con). In the next morning after evening exercising, fasting blood samples were obtained. Additional blood samples were
obtained 1–4 h after eating a given high-fat meal that based on participants_ body mass. Carbohydrate and fat oxidation rates were
measured before and after the meal. Results: After exercise, glucose and insulin concentrations decreased by 33% and 70% in MICE
compared with those in HIIE (P = 0.00–0.03). During the 1- to 2-h postprandial periods, the fat oxidation rate increased by 24%–37% in
HIIE that that in MICE and Con (P = 0.01–0.03); however, the carbohydrate oxidation rate was not significantly different among the
conditions (P = 0.28). During the postprandial period, insulin (P = 0.02–0.04) and triglyceride (P = 0.02–0.03) concentrations were lower
in HIIE than those in MICE and Con. No difference was observed in free fatty acid or the total areas under the curve of triglyceride and
free fatty acid among the conditions (P = 0.24–0.98). Conclusion: Acute MICE improved glucose and insulin metabolism immediately
after exercise. However, HIIE performed in the evening exerts more favorable effects than MICE for decreasing postprandial insulin and
triglyceride levels and increasing fat oxidation in the next morning. Key Words: EXERCISE INTENSITY, HIGH-FAT MEAL, LOW
VOLUME, TIME EFFICIENCY

R
ecent research has shown that postprandial lipemia
(PPL) is associated with increased risks of athero-
sclerosis (1) and cardiovascular disease (CVD) (2)
in adults. In an early study, Zilversmit (1) indicated that PPL
along with cholesterol (Chol), LDL cholesterol (LDL-C),
and very LDL cholesterol (VLDL) contributes to the posi-
tive association between hypertriglyceridemia and coronary
artery disease and the inverse relationship between HDL
cholesterol (HDL-C) and CVD. Research demonstrated that
the magnitude of PPL or single postprandial triglyceride
values can predict asymptomatic and symptomatic athero-
sclerosis, independent of risk factors measured in the fasting
state (3). The fasting PPL and postprandial triglyceride re-
sponses also correlated strongly with physical activity (4)
Address for correspondence: Chia-Lun Lee, Ph.D., Division of Physical and
Health Education, Center for General Education, National Sun Yat-sen
University, No. 70, Lienhai Rd., Kaohsiung City, Taiwan, ROC; E-mail:
karenlee1129@gmail.com.
Submitted for publication October 2017.
Accepted for publication March 2018.
0195-9131/18/5008-1687/0
MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ
Copyright Ó 2018 by the American College of Sports Medicine
DOI: 10.1249/MSS.0000000000001613
and dietary habit (5). Occasionally, a hectic day and a busy
working life may lead people to miss one meal a day (e.g.,
breakfast or dinner); the whole volume of the missed meal is
ingested with other meals on the same day. Hence, this type
of dietary behavior may be conducive to the ingestion of
high-fat food, which disturbs the natural lipid metabolism
(6). The ingestion of a high-fat meal (HFM) acutely changes
the blood lipid profile and reduces endothelial function for
many hours after the meal. Thus, a significant proportion of
life is spent in the postprandial state; the factors leading to
this transient impairment in endothelial function may play a
key role in the development of atherosclerosis (7).
PPL and aerobic exercise have been extensively demon-
strated to have antagonistic effects regarding cardiovascular
APPLIED SCIENCES
risk; aerobic exercise may decrease PPL, decreasing tri-
glyceride secretion by the liver and increasing plasma tri-
glyceride clearance by the muscle (6). However, the effect of
more intense exercise such as high-intensity interval exer-
cise (HIIE) (i.e., 85%–95% peak heart rate or 80%–100%
peak work rate) on PPL is not well understood. Sprint in-
terval exercise or HIIE has been proposed as a viable alter-
native to moderate-intensity continuous exercise (MICE)
because it is a time-efficient exercise strategy that elicits
improvements in the peak oxygen uptake (V̇O2peak) (8) and
muscle insulin sensitivity (9) in healthy adults. HIIE is

1687

Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 defined as near maximal efforts or submaximal interval ex-
ercise performed at an intensity of 85%–95% of the maximal
heart rate (HRmax); by contrast, sprint interval exercise is
characterized by efforts performed at intensities equal to or
greater than the intensity that elicits V̇O2peak, including all-
out or supramaximal efforts (10). An early study found that
an HIIE protocol involving 4  4 min activity at 85%–95%
HRmax or a matched work continuous exercise protocol at
60%–70% HRmax did not affect PPL triglyceride and HDL-C
levels on the next day (7). A 20-min bout of 4  30 s sprint
cycling also had no effect on PPL (11). By contrast, a 20-min
bout of 60  8 s sprint cycling against a fixed resistance at
60%–65% V̇O2max significantly decreased postprandial tri-
glyceride (12). Moreover, a study compared 3-min sessions at
115% anaerobic threshold with 1.5 min of recovery versus a
matched energy expenditure (EE) continuous exercise inter-
vention performed until an EE of 500 kcal was reached;
compared with moderate continuous exercise, the more in-
tense exercise intervention reduced PPL 2–4 h after HFM
(13). In addition, the HIIE intervention has been reported to
improve triglyceride concentration or triglyceride area under
the curve (AUC) (14–18), postprandial fat oxidation (19),
blood insulin sensitivity (16), and fat oxidation after 6-wk
sprint interval training (15). However, some studies have
compared the effects of single sessions of HIIE at different
intensities and for different durations on the PPL response;
these studies have found no significant effects on triglyceride
AUC (11,20–22) or that the HIIE results in more decreases in
PPL in girls than in boys (18).
A previous study found a higher reduction in postprandial
triglyceride in participants in the energy deficit condition
during a shortened postprandial protocol than during a lon-
ger postprandial protocol (16). Thus, EE and energy intake
(23) have been suggested to be important variables deter-
mining exercise-induced reductions in triglyceride during
submaximal interval exercise. Moreover, the time from ex-
ercise cessation to test meal consumption may play a role in
exercise-induced changes in PPL (24). Studies have provided
contradictory results regarding the effect of prior exercise on
PPL variations in the HIIE protocol. These contradictory results
may be attributed to interindividual variation, inconsistent en-
ergy intake after exercise, or insufficient time postexercise for
inducing an increase in lipoprotein lipase (LPL) activity. Ma-
nipulating energy intake through standardization at pre- and
postexercise intervals may reduce the variations in energy def-
APPLIED SCIENCES
icit and prolong the time for observing lipid metabolism. Re-
search has demonstrated that different intensities of the HIIE
protocol may not elicit similar effects on postprandial lipopro-
tein profile (11,12,14,17,20,22). Studies focused on the acute
effects of different exercise modes in PPL after HFM are im-
portant for developing a well-rounded exercise prescription to
reduce the risk of CVD in healthy individuals, as well as in the
sedentary population. Therefore, this study investigated the
effect of acute HIIE versus MICE on PPL at time points
ranging from immediately after exercise to the next day.
We hypothesized that HIIE can decrease PPL and produce
1688 Official Journal of the American College of Sports Medicine
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
a beneficial lipid profile compared with MICE in healthy
individuals.
METHODS
Participants and physical activity. A total of 36 healthy
and active men participated in this study. Participants were
25 T 5 yr old. The average height was 175 T 6 cm, the av-
erage body mass was 69 T 10 kg, and the average percentage
body fat was 12% T 4%. For this study, participants were
considered to perform ‘‘regular exercise’’ if they partici-
pated in approximately 60-min sessions of a structured ex-
ercise program that combined cardiovascular and resistance
exercise, at least three times per week for the past 3 yr.
Participants were recreationally active but were not for-
mally trained for any type of professional competition. The
exclusion criteria were as follows: smoking, anabolic ste-
roid intake, and a history of CVD, diabetes, hypertension, or
any other metabolic disease or illness requiring the inges-
tion of medications that affect carbohydrate or lipid me-
tabolism. All participants were fully informed of the aims,
risks, and discomfort associated with the investigation be-
fore providing written informed consent. This study was
approved by the Hospital institutional review board.
Initial assessment. To determine participants_ eligi-
bility, 5–7 d before their first familiarization session, fasting
blood samples (baseline) were collected for glucose, HDL-
C, LDL-C, VLDL, total Chol, and triglyceride measurement
to exclude participants presenting abnormal glucose, blood
lipids, or frank diabetes. Subsequently, participants_ skinfold
thickness was measured twice at three sites, namely, chest,
abdomen, and thigh, in rotational order (25). The measure-
ments were conducted to the nearest 0.1 mm on the right side
of the body by using Lange calipers (Cambridge Scientific
Industries, Inc., Cambridge, MD) and were used to determine
body composition. If the difference in measured values at
each site exceeded 1 mm, a third assessment was performed
by an experienced researcher certified as a health fitness in-
structor. These measured values were used to calculate body
density (25), which was then used to estimate the percentage
body fat [% body fat = (495 per density) j 450].
Experimental protocol. The randomized control de-
sign was used in this present study. Thirty-six participants
were randomly assigned to one of three experimental con-
ditions, including HIIE, MICE, and nonexercise control
(Con). At 7 d before the start of the study, each participant
reported to the laboratory for a familiarization session (i.e.,
HIIE and MICE). They also practiced a V̇O2peak test, be-
came accustomed to the gas collection equipment (e.g., gas
mask), and determined their preferred seat height on the er-
gometer. The three experimental conditions were as follows:
Con (n = 12), moderate-intensity exercise (MICE, n = 12),
and HIIE (n = 12). Each trial involved 2 d of diet and physical
activity controls, during which participants consumed a
laboratory-provided diet and performed no exercise outside
the laboratory. Participants refrained from physical activity
http://www.acsm-msse.org
and alcohol ingestion for 48 h before each trial and did not
consume any caffeine-containing beverage for 24 h before
each trial. Participants also recorded their diet 2 d before the
V̇O2peak test, and this was replicated during the subsequent
visit in exercise test.
On day 1, participants arrived at the laboratory at 3:30 PM
and rested for 10 min before their blood was collected from a
vein in the antecubital fossa. Subsequently, they consumed a
standardized meal for dinner at 4:00 PM. For all participants,
meals were consumed at a similar time on the test day. Par-
ticipants rested for 3 h after consuming a standardized meal.
At 7:00 PM, they performed 5 min warm-up and subsequently
completed one of the three exercise protocols, namely, HIIE,
MICE, or Con intervention. In the morning of day 2, participants
reported to the laboratory after a 12-h overnight fast. Upon ar-
rival at the laboratory, fasting blood samples were collected for
measurements of plasma glucose, triglyceride, insulin, HDL-C,
LDL-C, VLDL, total Chol, and free fatty acid (FFA). Im-
mediately after blood collection, resting EE, carbohydrate
oxidation, and fat oxidation were determined in the sitting
position. After completion of the fasting measurement,
participants consumed a test meal. Blood collection was repeated
hourly for 4 h postprandially, and resting EE, carbohydrate
oxidation, and fat oxidation measurements were repeated at 1,
2, 3, and 4 h postprandially. The protocol schematic is shown
in Figure 1.
Determination of V̇O2peak. One week before the first
trial, we determined the V̇O2peak of participants performing a
bicycle ramp protocol on an ergometric appliance (Cyclus 2;
RBM Elektronik-Automation GmbH, Leipzig, Germany).
After a 5-min warm-up period, each participant performed a
V̇O2peak test. Briefly, the workload was set at 50 W initially
and was then increased by 30 W every 1 min with the aim of
reaching each participant_s V̇O2peak. During the test, pul-
monary gas exchange and heart rate data were collected
using the Cortex Metamax 3B portable metabolic test system
(Cortex Biophysik, Leipzig, Germany) and wireless telemetry
system (Polar Electro, Kempele, Finland), respectively. Par-
ticipants were verbally encouraged to continue the maximal
cycling test until volitional fatigue. During the maximal pro-
tocol, V̇O2peak was determined within the final 30 s before
exhaustion. The highest values of oxygen uptake within the
final 30 s of the test were used for statistical analysis. The criteria
for V̇O2peak were as follows: (a) age-predicted maximum heart
FIGURE 1—Protocol schematic. HFM was consumed for breakfast.  represent capillary blood samples.
INTENSE EXERCISE ENHANCES LIPID OXIDATION
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
rate (208 j 0.7  age), (b) plateau in oxygen uptake that
increased by less than 150 mLIminj1 despite an increase
in power output, (c) RER greater than 1.10, and (d)
maximal capillary blood lactate concentration greater than
6 mmolILj1 after exercise. For all participants, at least three
of the four criteria were met. The coefficient of variation (CV)
for V̇O2peak for active populations in our laboratory was
2.6%. The O2 consumption (V̇O2) data collected at each
workload during the V̇O2peak test were further analyzed using
a simple linear regression to determine the exercise intensities
(i.e., 30%, 65%, and 85% V̇O2peak) of the MICE and HIIE
regimes. To verify metabolic commitment, the peak blood
lactate concentration was measured 5 min after cessation of
the exercise trial. Throughout the testing, oxygen uptake was
measured using an open-circuit breath-by-breath Spirograph,
and standard algorithms were used to dynamically account
for the time delay between gas consumption and volume
signal. The Spirograph was calibrated before each test by
using calibration gas (15% O2, 5% CO2; Praxair, Dusseldorf,
Germany) targeting the range of anticipated fractional gas
concentration; a precision 1-L syringe (nSpire, Oberthulba,
Germany) was used to inject the calibration gas. The regression
equation of oxygen consumption versus the work rate from the
V̇O2peak test and the determined V̇O2peak value was used to set
the work rates for HIIE and MICE, which corresponded to
85% and 65% V̇O2peak, respectively. Moreover, V̇O2 and CO2
production (V̇CO2) measurements from the V̇O2peak test were
used to determine the target EE for the exercise trial based on
the energy cost of cycling at high and moderate intensities.
Exercise protocols and EE. The HIIE protocol in-
volved repeated 10  60 s sprint cycling with pedaling as
fast as possible against a fixed resistance at 85% V̇O2peak,
interspersed with a 120-s active recovery at 30% V̇O2peak.
The MICE protocol involved 50 min of continuous endurance
exercise at 65% V̇O2peak, with a pedaling cadence of 60 or
70 rpm, as selected by the participant. The HIIE protocol was
chosen because it was well tolerated by our participants and did
not require longer intervals (2–4 min) or brief supramaximal
sprints (10–30 s in duration) (26). The nonexercise Con remained
in the laboratory during the entire period and expended little
energy (i.e., they watched a movie, read a book or magazine,
or worked on the computer).
Respiratory gases were collected before exercise and
during cycling on day 1, in the fasting condition before
APPLIED SCIENCES
Medicine & Science in Sports & Exercised 1689
 breakfast on day 2, and at 1, 2, 3, and 4 h after breakfast. The
parameters of V̇O2, V̇CO2, and RER were used to calculate
whole-body fat and carbohydrate oxidation. These calculations
were executed using the nonprotein RER table and the
following equations (27): carbohydrate oxidation = 4.210
(V̇CO2) j 2.962 (V̇O2); fat oxidation = 1.695 (V̇O2) j 1.701
(V̇CO2). To determine resting EE during the HFM test on day 2,
an indirect calorimeter was used to collect gas for 15 min after
10 min of rest in a sitting position.
Dietary recording and test meal. Participants were
instructed to maintain their usual diet throughout the study
period, and they recorded their food and drink intake and all
physical activities within 48 h before each test day. This
information was used to match their diet and activity patterns
across the V̇O2peak test and the one experimental condition.
The recorded food intake was analyzed by research staff
using a nutritional analysis software package (Nutritional
Chamberlain Line, Professional Edition, E-Kitchen Inc.,
Taiwan). The results were returned to participants so they
could mimic this intake on all days before test days.
On day 1, participants consumed a standardized meal,
which was devised depending on their body mass (daily
macronutrients: 60% carbohydrate, 23% fat, and 17% protein),
for dinner at 4:00 PM. The meal consisted of rice, chicken,
vegetables, eggs, and beans. Participants rested for 3 h after
dinner at 7:00 PM. Subsequently, they performed the acute
HIIE, MICE, or Con intervention. To avoid the ingestion of
extra food, they ate a small nutrition bar (25 g of carbohydrate,
14 g of fat, and 7 g of protein) at 08:30 PM. Before leaving the
laboratory on day 1, participants in each experimental condi-
tion were reminded that they could drink plain water but
should not consume any food.
For breakfast on day 2, the test meal consisted of bread,
cheese, peanut butter, margarine, and fruit juice. The calorie
composition size (kcal) of the HFM was determined based
on participants_ body mass. The calorie composition of the
meal was equal to 1.1 g of fat, 1.0 g of carbohydrate, and 0.3 g
of protein per kilogram of body mass, totaling approximately
13 kcalIkgj1 of body mass, similar to the meal used in the
study by Freese et al. (16). On the basis of the possible
mechanisms responsible for the reduction in postprandial
lipid metabolism, the breakfast meal was ingested approxi-
mately 12 h after exercise overnight. During the interval
between the breakfast meal ingested in the morning and
lunch 4 h later, no other meals or calorie-containing bever-
APPLIED SCIENCES
ages were allowed. Water was allowed in limited amounts.
Blood collection and analyses. Blood samples for
analyses were collected from the antecubital vein before the
exercise or control (i.e., no exercise) and immediately after
exercise on day 1. Additional blood samples were collected
before meal ingestion at 8:00 AM (i.e., after approximately 12 h
overnight fasting) and at 1, 2, 3, and 4 h after meal ingestion.
A 5-mL blood sample was collected in a tube containing a
serum clot activator (VacuetteÒ, St. Gallen, Switzerland) and
was centrifuged at 3000 rpm for 15 min at 4-C. The sample
was placed on ice during experiments and was stored frozen
1690 Official Journal of the American College of Sports Medicine
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
at j80-C. The collected serum was subsequently analyzed
for measuring insulin, triglyceride, total Chol, HDL-C, LDL-C,
VLDL, and FFA levels; the interassay CV values were 2.2%,
1.5%, 1.8%, 2.1%, 2.2%, 5.0%, and 2.1%, respectively. Se-
rum insulin levels were determined using a commercial kit
(DIAsource INS-IRMA kit, Nivelles, Belgium). Lipid pa-
rameters (triglyceride, total Chol, HDL-C, LDL-C, and
VLDL) were measured by photometric method (UnicelDxC
800, Beckman Coulter autoanalyzer). The serum FFA levels
were determined using a nonesterified fatty acid kit (Randox
Laboratories Canada Ltd., Ontario, Canada). All assays were
performed in duplicate on the first thaw. However, lactate and
glucose assays were performed once in a single analysis using
fresh whole blood. Blood lactate concentrations were mea-
sured immediately using an automated analyzer (Lactate Pro
TM LT-1730; Arkray KDK Corp., Kyoto, Japan), and blood
glucose concentrations were measured using a portable device
(Breeze2; Bayer, Munich, Germany); the interassay CV values
were 1.2% and 1.1%, respectively. Using the trapezoidal method,
postprandial responses for glucose, triglyceride, FFA, and insulin
were measured by summing the 17-h AUC for serum/plasma
concentration versus time (15). With n + 1 measurements yi at
time ti (i = 0, 1, 13, 14, 15, 16, and 17 h), the total AUC (TAUC,
mgIdLj1Ihj1; KUImLj1Ihj1; mmolILj1Ihj1) was calculated
as follows: 1  [(y0 + y1)/2] + 12  [(y1 + y2)/2] + 1  [(y2 +
y3)/2] + 1  [(y3 + y4)/2] + 1  [(y4 + y5)/2] + 1  [(y5 + y6)/2].
Statistical analysis. All data are presented as means T
SD. The Shapiro–Wilk normality test was applied to deter-
mine the homogeneity of all data. Preexercise, postexercise,
fasting, and postprandial plasma glucose, serum insulin,
triglyceride, Chol, FFA, HDL-C, LDL-C, and VLDL levels
were assessed using two-way repeated-measures ANOVA
for condition and condition–time interactions. Fasting and
postprandial V̇O2, V̇CO2, EE, carbohydrate oxidation, and
fat oxidation were also analyzed using two-way repeated-
measures ANOVA for condition–time interactions. The
Bonferroni post hoc correction was applied if a significant
difference was found. One-way ANOVA was used to com-
pare total EE and AUC (calculated using the trapezoidal
method) among the conditions. Statistical significance was
set at P e 0.05. The data were analyzed using SPSS for
Windows, Version 17.0 (SPSS, Chicago, IL). Informed by a
previous study detailing the changes in PPL after intense
interval cycling intervention in active healthy adults (16), we
hypothesized that triglyceride values would be more influenced
by different exercise regimes, and therefore, we expected to see
a 9% decrease on triglyceride in exercise regimes relatively to
control condition. Thus, our study had 80% power at a 0.05
significance level to detect a 9% decrease in triglyceride in the
exercise conditions. A sample size of 12 participants per con-
dition was required to detect the differences on the changes in
PPL profiles, including glucose, Chol, insulin, HDL-C, LDL-C,
triglyceride, and FFA, between experimental and control con-
ditions. Standardized effect sizes were also calculated using
Cohen equations (28) with the following threshold values: G0.2
(trivial); 90.2 and G0.6 (small); 90.6 and G1.2 (moderate); 91.2
http://www.acsm-msse.org
TABLE 1. Physical characteristics and fasting blood parameters of HIIE, MICE, and Con.
Metabolite HIIE (n = 12) MICE (n = 12) Con (n = 12) P d
Height (cm) 173 T 7 176 T 5 175 T 7 0.76 0.07
Weight (kg) 67 T 10 72 T 9 67 T 13 0.38 0.23
Body mass index (kgImj2) 22.3 T 2.4 23.3 T 3.1 21.8 T 2.9 0.38 0.35
Systolic BP (mm Hg) 127 T 5 127 T 7 128 T 9 0.92 0.14
Diastolic BP (mm Hg) 70 T 8 72 T 7 72 T 4 0.76 0.15
Body fat (%) 10.4 T 4.7 13.9 T 3.5 10.7 T 4.1 0.08 0.33
Blood glucose (mgIdLj1) 81 T 7 81 T 6 83 T 7 0.58 0.30
Insulin (KUImLj1) 6.7 T 1.6 8.4 T 3.5 7.1 T 2.3 0.32 0.17
Triglyceride (mgIdLj1) 48 T 11 58 T 24 52 T 18 0.43 0.05
Total cholesterol (mgIdLj1) 175 T 13 173 T 23 168 T 33 0.76 0.25
HDL-C (mgIdLj1) 68 T 12 62 T 17 64 T 17 0.67 0.06
LDL-C (mgIdLj1) 101 T 13 106 T 19 100 T 21 0.83 0.19
VLDL (mgIdLj1) 6.11 T 3.1 5.4 T 2.6 5.7 T 2.9 0.83 0.02
FFA (mmolILj1) 0.3 T 0.1 0.3 T 0.1 0.3 T 0.1 0.74 0.33
Values are expressed as mean T SD. BP, blood pressure.

and G2.0 (large); 92.0 and G4.0 (very large); and G4.0 nearly Metabolic rate and substrate utilization. The aver-
perfect (29). age premeal and postmeal values are reported in Table 2. Signif-
icant condition–time interactions were found for V̇O2 (P = 0.01,
RESULTS d = 0.6). The post hoc test indicated that the V̇O2 value of HIIE
was significantly higher than that of Con (P = 0.05). However, this
Physiological measurements and dietary in- value was not statistically different from that of MICE (P = 0.2).
take. Participants_ characteristics are presented in Table 1. No significant condition–time interaction (P = 0.33, d = 0.3) or
Participants in the three conditions had a normal range of blood main effect of condition (P = 0.79, d = 0.1) was found for V̇CO2.
pressure, body mass index, body fat, and blood lipid profile at During the postprandial period, no significant condition–time
the baseline. V̇O2peak values were not significantly different
among HIIE, MICE, and Con (48.2 T 6.3, 45.8 T 5.7, and 45.5 T
7.2 mLIkgj1Iminj1, respectively; P = 0.2, d = 0.3). During the TABLE 2. Metabolic rate before breakfast and during the postprandial period.
Metabolite HIIE (n = 12) MICE (n = 12) Con (n = 12)
exhaustion phase of the V̇O2peak test, the ratings of perceived
V̇O2 (LIminj1)
exertion were not significantly different among HIIE, MICE, Before meal 0.27 T 0.04 0.24 T 0.04 0.26 T 0.04
and Con (19 T 1, 19 T 1, and 18 T 1, respectively; P = 0.5, d = Postprandial 1 h 0.34 T 0.06* 0.30 T 0.03 0.29 T 0.05
0.4). Moreover, the peak heart rates were not significantly dif- Postprandial 2 h 0.33 T 0.05 0.31 T 0.03 0.30 T 0.03
Postprandial 3 h 0.32 T 0.06 0.30 T 0.03 0.29 T 0.04
ferent among HIIE, MICE, and Con (190 T 9, 190 T 16, and Postprandial 4 h 0.29 T 0.05 0.29 T 0.03 0.29 T 0.04
189 T 10 bpm, respectively; P = 0.9, d = 0.1). Blood lactate V̇CO2 (LIminj1)
Before meal 0.22 T 0.03 0.20 T 0.04 0.22 T 0.04
concentrations after the V̇O2peak test were not significantly Postprandial 1 h 0.27 T 0.06 0.25 T 0.03 0.24 T 0.05
different among HIIE, MICE, and Con (8.7 T 2.4, 9.8 T 2.8, Postprandial 2 h 0.26 T 0.05 0.25 T 0.02 0.24 T 0.03
and 9.3 T 3.6 mmolILj1, respectively; P = 0.2, d = j0.1). Postprandial 3 h 0.24 T 0.04 0.23 T 0.02 0.23 T 0.04
Postprandial 4 h 0.22 T 0.03 0.22 T 0.01 0.23 T 0.04
During the exercise intervention on day 1, the average heart RER
rate values were significantly different among HIIE, MICE, and Before meal 0.85 T 0.05 0.84 T 0.05 0.87 T 0.09
Postprandial 1 h 0.78 T 0.04*,** 0.84 T 0.02 0.85 T 0.07
Con (134 T 11, 138 T 12, and 68 T 8 bpm, respectively; P = 0.00, Postprandial 2 h 0.77 T 0.04 0.79 T 0.02 0.81 T 0.04
d = 6.2). During the HFM intervention on day 2, no significant Postprandial 3 h 0.75 T 0.04 0.78 T 0.05 0.78 T 0.07
Postprandial 4 h 0.76 T 0.03 0.76 T 0.05 0.78 T 0.06
condition–time interaction effect (P = 0.48, d = j0.3) and main EE (kcalIminj1)
effect of condition (P = 0.16, d = j0.4) were found for average Before meal 1.31 T 0.21 0.19 T 0.23 1.28 T 0.22
heart rates from premeal to postmeal. However, a main effect of Postprandial 1 h 1.64 T 0.32 1.47 T 0.19 0.41 T 0.27
Postprandial 2 h 1.59 T 0.28 1.51 T 0.17 1.45 T 0.19
time (P = 0.00, d = j1.3) showed that average heart rates during Postprandial 3 h 1.51 T 0.29 1.45 T 0.16 1.42 T 0.24
the postprandial 1–2 h had higher values compared with Postprandial 4 h 1.39 T 0.26 1.42 T 0.13 1.38 T 0.20
APPLIED SCIENCES
CHO oxidation rate (kJIminj1)
premeal, postprandial 3–4 h (premeal: 62 bpm; postprandial 1 h: Before meal 2.7 T 1.1 2.4 T 1.0 3.1 T 1.8
70 bpm; postprandial 2 h: 68 bpm; postprandial 3 h: 65 bpm; Postprandial 1 h 2.0 T 1.4 3.0 T 0.7 3.1 T 1.5
postprandial 4 h: 62 bpm, respectively). Postprandial 2 h 1.8 T 1.2 1.9 T 0.5 2.3 T 0.9
Postprandial 3 h 1.3 T 1.0 1.6 T 1.0 1.6 T 1.7
During the 48 h before day 2, the estimated average energy Postprandial 4 h 1.3 T 0.6 1.2 T 1.0 1.7 T 1.5
intake levels were similar among HIIE, MICE, and Con (10.6 T Fat oxidation rate (kJIminj1)
Before meal 2.5 T 1.5 2.4 T 0.8 2.1 T 1.6
1.2, 10.8 T 1.3, and 11.0 T 1.6 MJIdj1, respectively). Moreover, Postprandial 1 h 4.6 T 0.8*,** 2.9 T 0.6 2.6 T 1.3
during the aforementioned period, the macronutrient intake Postprandial 2 h 4.6 T 1.1* 4.1 T 0.7 3.5 T 0.9
levels were similar among HIIE, MICE, and Con (protein: 108 T Postprandial 3 h 5.0 T 1.4 4.2 T 1.3 4.1 T 1.5
Postprandial 4 h 4.3 T 1.2 4.5 T 1.3 3.9 T 1.4
22 vs 110 T 23 vs 112 T 25 gIdj1; carbohydrate: 380 T 42 vs
Values are expressed as mean T SD. CHO, carbohydrate.
387 T 45 vs 394 T 53 gIdj1; fat: 65 T 15.4 vs 66 T 14.3 vs 67 T *Significantly different from Con (P G 0.05).
15.8 gIdj1). **Significantly different from MICE (P G 0.05).

INTENSE EXERCISE ENHANCES LIPID OXIDATION Medicine & Science in Sports & Exercised 1691

Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 interaction (P = 0.07, d = j0.6) was found for RER; how-
ever, a main effect of condition was found for RER (P = 0.02,
d = j0.8). The post hoc test indicated that at the 1-h post-
prandial time point, RER was significantly lower in HIIE
than that in Con (P = 0.00) and MICE (P = 0.01). A main
effect of time was found for all metabolic rates and substrate
partitioning values (P = 0.00).
A significant main effect of condition was found for exercise
EE per minute among HIIE, MICE, and Con (11.0 T 2.1 vs
12.2 T 1.7 vs 1.45 T 0.21 kcalIminj1; P = 0.00, d = 6.4). The
post hoc test showed that EE values in both HIIE and MICE
were significantly higher than those in Con (P = 0.00), but
HIIE was not different from MICE (P = 0.22). However, total
EE for the exercise session was significantly different be-
tween HIIE and MICE (330 T 64 vs 610 T 85 kcal; P = 0.00,
d = 8.6). During the HFM test on day 2, significant condition–
time interaction (P = 0.03, d = 0.5) was found for EE;
however, post hoc showed that no significant difference (P =
0.1–0.95) before an HFM meal and during the postprandial
period among HIIE, MICE, and Con (Table 2).
The results show that there was a significant condition–time
interaction for fat oxidation rate (P = 0.02, d = 0.64). The
post hoc test showed that at the 1-h postprandial time point, the
fat oxidation rate was significantly higher in HIIE than that in
MICE and Con (P = 0.00). Moreover, at the 2-h postprandial
time point, the fat oxidation rate was significantly higher in
HIIE than that in Con (P = 0.02). No significant difference was
observed between MICE and Con (P = 1.00). On the other hand,
no significant condition–time interaction (P = 0.44, d = j0.3)
or main effect of condition (P = 0.3, d = j0.23) was found
for the carbohydrate oxidation rate. However, a main effect of
time (P = 0.00, d = j1.85) was found for HIIE and MICE.
Changes in blood parameters in response to
exercise. Significant differences were observed in the
condition–time interactions for blood glucose (P = 0.00, d = 0.15),
Chol (P = 0.00, d = 1.92), insulin (P = 0.00, d = 1.26), HDL-C
(P = 0.00, d = 0.08), and LDL-C (P = 0.00, d = 1.19), as
illustrated in Figures 2A, 2B, 2D, 2E, and 2F, respectively.
However, according to post hoc test results, only HDL-C did
not significantly differ among the conditions. After exercise,
the glucose level was markedly lower in MICE than that in
Con (17%, P = 0.02) and HIIE (33%, P = 0.03). After exercise,
the Chol level was higher in HIIE than that in Con (19%,
P = 0.01), and the Chol level tends to increase in MICE
compared with Con (13%, P = 0.06). After exercise, the insulin
APPLIED SCIENCES
level in MICE was different from that in Con (65%, P = 0.00) and
HIIE (70%, P = 0.00). However, on day 2, the insulin
level in HIIE was lower than that in Con before the meal
(30%, P = 0.03) and that in MICE at the 3-h postprandial time
point (43%, P = 0.02).
A significant condition–time interaction effect (P = 0.02,
d = j0.4) was found for the triglyceride level. The post hoc
test showed that at 4 h after HFM, the triglyceride level in HIIE
decreased to approximately 53% and 46% compared with those
in MICE (P = 0.02) and Con (P = 0.03), respectively. More-
over, the percentage changes in triglyceride levels from
1692 Official Journal of the American College of Sports Medicine
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
premeal to 4 h postmeal did not differ significantly among the
conditions (HIIE vs MICE vs Con; 110% T 76% vs 213% T
261% vs 216% T 210%, P = 0.34, d = j0.27).
No significant interaction effect (P = 0.54, d = 0.08) or
main effect of condition (P = 0.74) was found for FFA.
However, significant differences were observed in the main
effect of time (P = 0.00) for FFA. This finding indicated that
after HFM intake, FFA progressively increased during the
postprandial period. The percentage change from premeal to
the 4-h postprandial time point revealed a significant difference
in FFA among the conditions (HIIE vs MICE vs Con; 30% T
50% vs 29% T 68% vs 115% T 142%, P = 0.05, d = j0.89).
The post hoc test showed a trend to reach significant difference
in HIIE and MICE compared with Con (P = 0.08).
Regarding the lipemic response, glucose TAUC (P = 0.00,
d = j0.27) and insulin TAUC (P = 0.00, d = j0.9) were
significantly different among the conditions. The post hoc test
showed that glucose TAUC and insulin TAUC were signifi-
cantly lower in MICE than those in HIIE (P = 0.00) and Con
(P = 0.00). However, no significant difference was observed
in triglyceride TAUC (P = 0.98, d = j0.01) or FFA TAUC
(P = 0.24, d = 0.09) among HIIE, MICE, and Con (Table 3).
DISCUSSION
The main purpose of this investigation was to determine
the effectiveness of a single session of high-intensity interval
cycling and a single session of continuous moderate-intensity
cycling for blood lipemia profiles during rest and postprandial
periods. The main finding of this study is that blood glucose
and insulin concentrations were higher in HIIE than those in
MICE immediately after exercise. LDL-C and Chol concen-
trations in HIIE increased compared with those in Con and
MICE. However, after HFM intake, insulin and triglyceride
concentrations in HIIE decreased compared with those in
MICE or Con. Triglyceride TAUC and FFA TAUC did not
change in response to the HIIE and MICE interventions.
Moreover, compared with MICE and Con, fat oxidation rate in
HIIE significantly increased to 27%–43% after HFM intake.
Previous studies have reported that increased PPL is associated
with an increased risk of CVD (2,30). Thus, comparing the
efficacy of different interventions in reducing postprandial
triglyceride concentration and determining the variations in
physiological parameters after the interventions are worthwhile.
A previous study demonstrated that during the postprandial
period after exercise, a high-intensity exercise intervention
results in higher oxygen consumption and lipid oxidation than
a matched low-intensity intervention with equivalent EE (31).
However, in the present study, during the 1- to 2-h post-
prandial period, V̇ O2 and fat oxidation rate were higher and
RER was lower in HIIE than those in MICE, although the two
exercise regimes were not isocaloric. These parameters also
differed between HIIE and Con. The EE of the HIIE interven-
tion was significantly lower than that of the MICE intervention
(279 T 60 vs 513 T 80 kcal, P = 0.00, d = 2.7). Hence, in
addition to the effect of equal EE during exercise on PPL (13),
http://www.acsm-msse.org
FIGURE 2—Mean blood glucose (A), cholesterol (B), triglyceride (C), insulin (D), HDL-C (E), and LDL-C (F) at preexercise, postexercise, premeal,
and postprandial period. *Significantly different between HIIE and Con (P G 0.05). †Significantly different between MICE and Con (P G 0.05).
‡Significantly different between HIIE and MICE (P G 0.05). §Significantly different across time (P G 0.05). a, change over time in HIIE; b, change over
time in MICE; c, change over time in Con. The line denotes the separation between day 1 and day 2.

there have been some indications that exercise intensity plays an exercise for longer duration can cause a substantial net reduc-
important role in PPL responses (19,31). The present study used tion in muscle glycogen content; moreover, exercise-induced
an exercise intensity of 65% V̇O2peak for 50 min as the protocol muscle glycogen depletion has been shown to activate glyco-
for the MICE intervention (MICE: 152 T 26 W) and of 85% gen synthase and increase muscle oxidative capacity (9). Our
V̇O2peak for 20 min with 10 min interspersed rest as the pro- finding is consistent with that of a previous study (19), in which
tocol for the HIIE intervention (248 T 42 W). The exercise postprandial fat oxidation was higher in the isoenergetic high-
APPLIED SCIENCES
intensity in the HIIE intervention differed from that in the intensity exercise intervention (a 2-min intense exercise at 90%
MICE intervention. Highly intense exercise or lower-intensity V̇O2peak with 2-min rest for a total exercise time of 42 min) than
that in moderate-intensity exercise intervention (50% V̇O2peak for
TABLE 3. TAUC responses of serum/plasma glucose, insulin, triglyceride, and FFA.
60 min). Nevertheless, the time of each exercise trial and the
Condition HIIE (n = 12) MICE (n = 12) Con (n = 12)
total exercise time in the previous study (19) were longer than
Glucose (mgIdLj1 per 17 h) 1649 T 142** 1432 T 123* 1576 T 119
ours. The protocols for the exercise regimes were established
Insulin (KUImLj1 per 17 h) 245 T 70** 171 T 64* 273 T 79 under the consideration of time-efficient exercise. Thus, during
Triglyceride (mgIdLj1 per 17 h) 1376 T 880 1424 T 708 1408 T 574 each training session, only approximately 10 min of exercise
FFA (mmolILj1 per 17 h) 7.5 T 1.6 9.1 T 2.1 8.1 T 2.9
was performed over a 15- to 30-min period (9). The HIIE in-
Values are expressed as mean T SD.
*Significantly different from Con (P G 0.05).
tervention increased postprandial V̇O2 and fat oxidation and
**Significantly different from MICE (P G 0.05). reduced RER, although no change was observed in EE or the

INTENSE EXERCISE ENHANCES LIPID OXIDATION Medicine & Science in Sports & Exercised 1693

Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 carbohydrate oxidation rate in active men performing this in-
tervention. Thus, HIIE is more effective for increasing the fat
oxidation during postprandial period than MICE. Given the
greater improvement in postprandial RER and fat oxidation af-
ter HIIE in the current study, exercise intensity may be an im-
portant mediator of PPL responses, and high-intensity exercise
offers a low-volume alternative to moderate-intensity exercise.
In the present study, after a single session of exercise
without subsequent meal intake, blood glucose and insulin con-
centrations in MICE decreased compared with those in HIIE and
Con (Figs. 2A and 2D). Moderate-intensity endurance exercise
results in muscle contractions that improve insulin-mediated
glucose uptake; moreover, exercise increases glucose transport
capacity in muscle membrane but simultaneously increases
glucose delivery through increased muscle blood flow, in addi-
tion to increased enzymatic activity related to glucose metabo-
lism (32). Decreases in blood glucose and insulin concentrations
immediately after exercise might be attributed to rapid increases
in glucose transporter 4 expression, which in turn potentiates
insulin-stimulated glucose transport capacity; thus, these decreases
may provide a survival advantage by inducing the more rapid
replenishment of muscle glycogen stores (33). Furthermore, re-
garding lipid metabolism, elevated LDL-C and Chol levels after
exercise might be mediated by A-adrenergic stimulation. In the
present study, we did not measure the epinephrine concentra-
tion in the exercise conditions. However, based on previous
work, elevations in plasma epinephrine and norepinephrine
concentrations immediately after endurance exercise or HIIE
(34) may increase whole-body lipolysis. Therefore, increases
in fat oxidation induced by a high-intensive cycling exercise
might attribute to the activations of adrenalin and LPL (35).
The two interventions had similar effects on PPL (i.e., HDL-C,
LDL-C, VLDL, Chol, and FFA), except for insulin and triglyc-
eride. This discrepancy is likely because most parameters of PPL
did not rapidly change in response to the acute HIIE and MICE
interventions. The lack of changes in lipemic responses including
FFA, Chol, HDL-C, LDL-C, and VLDL on day 2 during the
postprandial period may partially explain the unaltered LPL
activity after acute exercise (36). In general, the regulation of
LPL may be complex because exercise (35), feeding, and fasting
(37) have been individually shown to have antagonistic effects.
Furthermore, although the exercise-induced regulation of muscle
LPL expression may be pretranslational, LPL regulation in adi-
pose tissue under different conditions has been shown to be
transcriptional, translational, and posttranslational (35). In
APPLIED SCIENCES
addition, exercise duration or postexercise period until HFM
consumption maybe factors affecting LPL activity. A study
confirmed a decrease in VLDL and an increase in FFA at 4.5 h
after exercising for 90 min at 58% T 5% V̇O2max (38). Another
study directly compared endurance exercise (60%–65% V̇O2max
with 60 min) with resistance exercise (3 sets and 10 repetitions
of each exercise at 90%; a maximum time of approximately
60 min) and investigated their effects on postprandial FFA
metabolism. Compared with the control trial, the exogenous
plasma FFA content increased significantly after the ingestion
of a liquid test meal after the endurance and resistance
1694 Official Journal of the American College of Sports Medicine
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
exercise; however, no significant difference in total plasma
FFA was observed between endurance and control trials (39).
The present results are consistent with those of previous stud-
ies, in which the total FFA concentration either immediately
after exercise (34) or during the postprandial period (39,40)
did not change between the experimental conditions; FFA
TAUC also did not change.
Acute high-intensity interval cycling exercise decreased
insulin and triglyceride concentrations 3 and 4 h after HFM,
respectively. Nevertheless, these changes that temporarily
appeared were lower in HIIE than those in Con and MICE.
Compared with Con and MICE, the insulin concentration in
HIIE decreased significantly by approximately 33% and 40%,
respectively, at the 3-h postprandial time point. A previous study
found improvements in insulin sensitivity at 14 d after the final
bout of high-intensity cycle exercise on an ergometer (41), and the
improvements were ascribed to chronic training adaptations (9).
Insulin is known to play a pivotal role in triglyceride metabolism.
It regulates triglyceride uptake in skeletal muscle and adipose
tissue and VLDL release from the hepatic tissue. Insulin sen-
sitivity is also an important biomarker of type 2 diabetes and
metabolic syndrome, and it is a primary target for preventative
intervention (42). In the present study, insulin sensitivity from
the preexercise to the 4-h postprandial time points was calculated
using the McAuley index (43) (data not shown). However, we
found that insulin sensitivity was higher in HIIE than that in
MICE, with a strong trend observed at the 4-h postprandial time
point (2.30 T 0.12 vs 2.12 T 0.21, P = 0.06). No differences were
also observed between either HIIE and Con (P = 0.12) or MICE
and Con (P = 0.93) for the McAuley index at 4 h postprandial
time point. The HIIE intervention may decrease the insulin
concentration and improve insulin sensitivity during the post-
prandial period. These effects may be because skeletal muscle
contractions cause the transport of glucose transporter 4 mole-
cules to the cell membrane and increase glucose and triglyceride
uptake in an intensity-dependent manner. As mentioned, the
transient increase in postprandial triglyceride after the ingestion
of a meal rich in fat may be a more favorable predictor of CVD.
Compared with MICE and Con, triglyceride was significantly
decreased to 46%–53% in HIIE at the 4-h postprandial time
point. This finding indicates that the HIIE intervention is more
effective than the MICE and Con interventions in decreasing
triglyceride. Consistent evidence shows that performing repeated
HIIE at an intensity of 85%–90% V̇O2peak for ~12–16 h before
HFM ingestion can reduce PPL in healthy people (14,18,19). By
contrast, previous studies have shown that acute low-volume
HIIE cycling performed 12 h before HFM ingestion cannot re-
duce triglyceride TAUC over a 4-h postprandial period in
healthy men (18,20). The reason for the lack of effects of this
exercise protocol is unclear, although several suggestions can be
made. For example, because PLP data were not collected over a
period longer than 4 h after HFM ingestion, changes during the
later period may not be able to be perceived. The result for the
triglyceride TAUC during the postprandial period of 4 h differs
from that during the postprandial period of approximately 6.5 h
used in other studies (14,21).
http://www.acsm-msse.org
 A possible limitation of this study is the variation between
participants in the conditions. This study used the randomized
control design to determine the effects of HIIE and MICE on
the PPL responses in healthy and active population. Fortunately,
the characteristics of our participants at baseline, i.e., initial fit-
ness level, exercise experiences and habits, blood parameters,
and dietary intake before exercise test, were not significantly
different among conditions. In addition, the familiarization trial
for HIIE or MICE was performed to reduce any learning effects
before the formal experiment. These data might partly attenuate
the effect of interindividual variation. However, further studies
with crossover design are needed to clarify the effects of HIIE or
MICE on the postprandial lipoprotein profile.
In conclusion, compared with the HIIE and Con interventions,
the acute MICE intervention reduces insulin levels after exercise
and decreases insulin TAUC. Thus, the MICE intervention has a
positive effect on glucose and insulin metabolism. However, the
HIIE intervention induces greater decreases in postprandial
REFERENCES
1. Zilversmit DB. Atherogenesis: a postprandial phenomenon. Circulation.
1979;60(3):473–85.
2. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A.
Nonfasting triglycerides and risk of myocardial infarction, ische-
mic heart disease, and death in men and women. JAMA. 2007;
298(3):299–308.
3. Patsch W, Esterbauer H, Foger B, Patsch JR. Postprandial lipemia
and coronary risk. Curr Atheroscler Rep. 2000;2(3):232–42.
4. Homer AR, Fenemor SP, Perry TL, et al. Regular activity breaks
combined with physical activity improve postprandial plasma tri-
glyceride, nonesterified fatty acid, and insulin responses in healthy,
normal weight adults: a randomized crossover trial. J Clin Lipidol.
2017;11(5):1268–1279.e1.
5. Emerson SR, Kurti SP, Teeman CS, et al. Realistic test-meal
protocols lead to blunted postprandial lipemia but similar inflam-
matory responses compared to a standard high-fat meal. Current
Developments in Nutrition. 2017;1(4):e00232.
6. Katsanos CS. Prescribing aerobic exercise for the regulation of
postprandial lipid metabolism: current research and recommenda-
tions. Sports Med. 2006;36(7):547–60.
7. Tyldum GA, Schjerve IE, TjLnna AE, et al. Endothelial dysfunction
induced by post-prandial lipemia: complete protection afforded by
high-intensity aerobic interval exercise. J Am Coll Cardiol. 2009;
53(2):200–6.
8. Milanovic Z, Sporis G, Weston M. Effectiveness of high-intensity
interval training (HIT) and continuous endurance training for V̇O2max
improvements: a systematic review and meta-analysis of controlled
trials. Sports Med. 2015;45(10):1469–81.
9. Gillen JB, Gibala MJ. Is high-intensity interval training a time-
efficient exercise strategy to improve health and fitness? Appl
Physiol Nutr Metab. 2014;39(3):409–12.
10. MacInnis MJ, Gibala MJ. Physiological adaptations to interval train-
ing and the role of exercise intensity. J Physiol. 2017;595(9):2915–30.
11. Tan MS, Mok A, Yap MC, Burns SF. Effect of sprint interval
versus continuous cycling on postprandial lipaemia. J Sports Sci.
2013;31(9):989–95.
12. Tan M, Chan Moy Fat R, Boutcher YN, Boutcher SH. Effect of high-
intensity intermittent exercise on postprandial plasma triacylglycerol
in sedentary young women. Int J Sport Nutr Exerc Metab. 2014;
24(1):110–8.
INTENSE EXERCISE ENHANCES LIPID OXIDATION
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
insulin and triglyceride concentrations and greater increases in
fat oxidation than the MICE and Con interventions. Therefore,
a single session of HIIE in the evening exerts more favorable
effects than continuous moderate-intensity exercise for decreas-
ing insulin and triglyceride levels and increasing postprandial fat
oxidation in the next morning. Because much of human life is
spent in the postprandial state, these findings are of significance
for the reduction of CVD risk and offer insight into the important
mechanisms through which exercise reduces the risk.
The authors thank all the participants for their active participation
and Mr. Shih-Feng Ting for his assistance with the testing procedure.
The authors also thank the Polypact International Co., Ltd., for spon-
soring the consumable materials used for the Cortex metabolic analysis
system. The results of the study are presented clearly, honestly, and
without fabrication, falsification, or inappropriate data manipulation, and
do not constitute. This study was supported by a grant from the Ministry
of Science and Technology, Taiwan (MOST 105-2410-H-110-042).
The authors declare no conflicts of interest or source of funding in
this study. The results of the present study do not constitute endorse-
ment by the American College of Sports Medicine.
13. Ferreira AP, Ferreira CB, Souza VC, et al. The influence of intense
intermittent versus moderate continuous exercise on postprandial
lipemia. Clinics (Sao Paulo). 2011;66(4):535–41.
14. Thackray AE, Barrett LA, Tolfrey K. Acute high-intensity interval
running reduces postprandial lipemia in boys. Med Sci Sports
Exerc. 2013;45(7):1277–84.
15. Freese EC, Gist NH, Acitelli RM, et al. Acute and chronic ef-
fects of sprint interval exercise on postprandial lipemia in women
at-risk for the metabolic syndrome. J Appl Physiol (1985). 2015;
118(7):872–9.
16. Freese EC, Levine AS, Chapman DP, Hausman DB, Cureton KJ.
Effects of acute sprint interval cycling and energy replacement on
postprandial lipemia. J Appl Physiol (1985). 2011;111(6):1584–9.
17. Gabriel BM, Pugh J, Pruneta-Deloche V, Moulin P, Ratkevicius A,
Gray SR. The effect of high intensity interval exercise on post-
prandial triacylglycerol and leukocyte activation–monitored for 48 h
post exercise. PLoS One. 2013;8(12):e82669.
18. Bond B, Williams CA, Isic C, et al. Exercise intensity and post-
prandial health outcomes in adolescents. Eur J Appl Physiol.
2015;115(5):927–36.
19. Trombold JR, Christmas KM, Machin DR, Kim IY, Coyle EF.
Acute high-intensity endurance exercise is more effective than
moderate-intensity exercise for attenuation of postprandial triglyceride
elevation. J Appl Physiol (1985). 2013;114(6):792–800.
20. Allen E, Gray P, Kollias-Pearson A, et al. The effect of short-duration
sprint interval exercise on plasma postprandial triacylglycerol levels in APPLIED SCIENCES
young men. J Sports Sci. 2014;32(10):911–6.
21. Thackray AE, Barrett LA, Tolfrey K. High-intensity running and
energy restriction reduce postprandial lipemia in girls. Med Sci
Sports Exerc. 2016;48(3):402–11.
22. Panissa VL, Julio UF, Diniz TA, et al. Postprandial lipoprotein
profile in two modes of high-intensity intermittent exercise. J Exerc
Rehabil. 2016;12(5):476–82.
23. Maraki MI, Sidossis LS. The latest on the effect of prior exercise
on postprandial lipaemia. Sports Med. 2013;43(6):463–81.
24. Silvestre R, Kraemer WJ, Quann EE, et al. Effects of exercise at
different times on postprandial lipemia and endothelial function.
Med Sci Sports Exerc. 2008;40(2):264–74.
25. Heyward VH, Gibson AL. Advanced Fitness Assessment and Exercise
Prescription. Champaign (IL): Human Kinetics; 2014.
Medicine & Science in Sports & Exercised 1695
 26. Weston M, Taylor KL, Batterham AM, Hopkins WG. Effects of
low-volume high-intensity interval training (HIT) on fitness in
adults: a meta-analysis of controlled and non-controlled trials.
Sports Med. 2014;44(7):1005–17.
27. Jeukendrup AE, Wallis GA. Measurement of substrate oxidation
during exercise by means of gas exchange measurements. Int J
Sports Med. 2005;26(1 Suppl):S28–37.
28. Cohen J. Statistical Power Analysis for the Behavioral Sciences.
New York: Academic Press, Inc.; 1988.
29. Hopkins WG. A scale of magnitudes for effect statistics [Internet].
2002 [cited 2018 Jan 03]. Available from http://sportsciorg/resource/
stats/effectmaghtml.
30. Pirillo A, Norata GD, Catapano AL. Postprandial lipemia as a
cardiometabolic risk factor. Curr Med Res Opin. 2014;30(8):1489–503.
31. Yoshioka M, Doucet E, St-Pierre S, et al. Impact of high-intensity
exercise on energy expenditure, lipid oxidation and body fatness.
Int J Obes Relat Metab Disord. 2001;25(3):332–9.
32. Richter EA, Derave W, Wojtaszewski JF. Glucose, exercise and
insulin: emerging concepts. J Physiol. 2001;535(Pt 2):313–22.
33. Ren JM, Semenkovich CF, Gulve EA, Gao J, Holloszy JO. Exercise
induces rapid increases in GLUT4 expression, glucose transport
capacity, and insulin-stimulated glycogen storage in muscle. J Biol
Chem. 1994;269(20):14396–401.
34. Williams CB, Zelt JG, Castellani LN, et al. Changes in mechanisms pro-
posed to mediate fat loss following an acute bout of high-intensity interval
and endurance exercise. Appl Physiol Nutr Metab. 2013;38(12):1236–44.
35. Seip RL, Angelopoulos TJ, Semenkovich CF. Exercise induces
human lipoprotein lipase gene expression in skeletal muscle but not
adipose tissue. Am J Physiol. 1995;268(2 Pt 1):E229–36.
APPLIED SCIENCES
1696 Official Journal of the American College of Sports Medicine
Copyright © 2018 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
36. Grandjean PW, Crouse SF, Rohack JJ. Influence of cholesterol
status on blood lipid and lipoprotein enzyme responses to aerobic
exercise. J Appl Physiol (1985). 2000;89(2):472–80.
37. Doolittle MH, Ben-Zeev O, Elovson J, Martin D, Kirchgessner TG.
The response of lipoprotein lipase to feeding and fasting. Evi-
dence for posttranslational regulation. J Biol Chem. 1990;265(8):
4570–7.
38. BLrsheim E, Knardahl S, HLstmark AT. Short-term effects of ex-
ercise on plasma very low density lipoproteins (VLDL) and fatty
acids. Med Sci Sports Exerc. 1999;31(4):522–30.
39. Davitt PM, Arent SM, Tuazon MA, Golem DL, Henderson GC.
Postprandial triglyceride and free fatty acid metabolism in obese
women after either endurance or resistance exercise. J Appl Physiol
(1985). 2013;114(12):1743–54.
40. Trilk JL, Singhal A, Bigelman KA, Cureton KJ. Effect of sprint
interval training on circulatory function during exercise in seden-
tary, overweight/obese women. Eur J Appl Physiol. 2011;111(8):
1591–7.
41. Richards JC, Johnson TK, Kuzma JN, et al. Short-term sprint interval
training increases insulin sensitivity in healthy adults but does not af-
fect the thermogenic response to beta-adrenergic stimulation. J Physiol.
2010;588(Pt 15):2961–72.
42. Little JP, Gillen JB, Percival ME, et al. Low-volume high-intensity
interval training reduces hyperglycemia and increases muscle mito-
chondrial capacity in patients with type 2 diabetes. J Appl Physiol
(1985). 2011;111(6):1554–60.
43. Gutch M, Kumar S, Razi SM, Gupta KK, Gupta A. Assessment
of insulin sensitivity/resistance. Indian J Endocrinol Metab. 2015;19(1):
160–4.
http://www.acsm-msse.org