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Hourly 4-s Sprints Prevent Impairment of
Postprandial Fat Metabolism from Inactivity
ANTHONY S. WOLFE, HEATH M. BURTON, EMRE VARDARLI, and EDWARD F. COYLE
Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, TX
ABSTRACT
WOLFE, A. S., H. M. BURTON, E. VARDARLI, and E. F. COYLE. Hourly 4-s Sprints Prevent Impairment of Postprandial Fat Metabolism
from Inactivity. Med. Sci. Sports Exerc., Vol. 52, No. 10, pp. 2262–2269, 2020. High postprandial plasma lipids (PPL; i.e., triglycerides) are a
risk factor for cardiovascula r disease. Physical inactivity, characterized by prolonged s itting and a low step count, elevates PPL and thus risk of
disease. Purpose: This study determined if the interruption of prolonged sitting (i.e., 8 h of inactivity) with hourly cycling sprints of only 4-s
duration each (i.e., 4 s 5perhour8h=160s·d
−1
SPRINTS) improves PPL. The 4-s sprints used an inertial load ergometer and were
followed by 45 s of seated rest. Methods: Four men and four women participated in two trials. Interventions consisted of an 8-h period of
sitting (SIT), or a trial with equal sitting time interrupted with five SPRINTS every hour. The morning after the interventions, PPL and fat
oxidation were measured over a 6-h period. Plasma glucose, insulin, and triglyceride concentrations were measured bihourly and incremental
area under the curve(AUC) was calculated. Results: No differences (P> 0.05) between interventions were found for plasma insulin or glucose
AUC. However, SPRINTS displayed a 31% (408 ± 119 vs 593 ± 88 mg·dL
−1
per 6 h; P= 0.009) decrease in plasma triglyceride incremental
AUC and a 43% increase inwhole-body fat oxidation (P= 0.001) when compared with SIT.Conclusions: These data indicate that hourly very
short bouts (4 s) of maximal intensity cycle sprints interrupting prolonged sitting can significantly lower the next day’s postprandial plasma
triglyceride response and increase fat oxidation after a high-fat meal in healthy youngadults. Given that these improvements were elicitedfrom
only 160 s of nonfatiguing exercise per day, it raises the question as to what is the least amount of exercise that can acutely improve fat me-
tabolism and other aspects of health. Key Words: PROLONGED SITTING, LIPEMIA, INERTIAL LOAD ERGOMETER
Over the past several decades, people living in modern
societies have become more and more physically in-
active because of technological innovations that have
greatly increased “screen time”and reduced the need to move
(1–3). As a result, people are spending an increasing amount
of time sitting throughout the waking hours, and they are
doing so with long periods that are devoid of meaningful
physical activity. Physical inactivity impairs cardiometa-
bolic health, and it is estimated to cause 16% of all deaths,
largely through cardiovascular disease (2–4).
The identification of effective activity/exercise programs to
counteractperiods of inactivity from prolonged sitting is ongo-
ing. One alarming statistic indicates that people who meet the
recommended level of exercise (i.e., 150 min·wk
−1
of moder-
ate intensity [5,6]) are still at elevated risk of cardiovascular
disease if they sit for prolonged periods throughout the day
(2–4). A large epidemiological study (3), estimated that in
order to counteract the effects of prolonged sitting, a person
needs to exercise for 60–75 min·d
−1
at moderate intensity. Fur-
thermore, recent work by Kim et al. (7) and Akins et al. (8) re-
ported that 60 min of running (e.g., 63%–67% V
˙
O
2max
)failed
to improve postprandial lipemia after several days of sitting for
13.5 h·d
−1
, a condition termed “exercise resistance.”There-
fore, it seems impractical to explore exercise bouts of longer
than 1 h·d
−1
to counteract the cardiometabolic risk of pro-
longed sitting due to adherence problems in the general popu-
lation. Furthermore, the main reason people give for being
inactive is lack of time to move and/or exercise throughout
the day (9).
Another approach is to interrupt prolonged sitting with peri-
odic bouts of activity/exercise throughout the day. Walking for
1–3 min every 15–30 min has been found to improve post-
prandial glucose metabolism on the day of the 1- to 3-min
bouts, yet it did not improve postprandial lipemia (10–12).
However, a recent study using the same protocol found post-
prandial lipemia to be improved the next day, agreeing with
the idea that it takes 12–24 h for the effects of activity/
exercise to be manifested in improved lipid metabolism (13).
Given that people claim a major reason for not being phys-
ically active or exercising is lack of time (9), it follows that a
mode of exercise, which is as brief as possible, should be in-
vestigated. Very brief exercise performed with maximal effort
has the advantage of being capable of producing very-high-
power outputs and thus activation of a large mass of muscle.
When sprints are performed maximally, both type I and type
Address for correspondence: Edward F. Coyle, Ph.D., Human Performance
Laboratory, Department of Kinesiology and Health Education, University
of Texas at Austin, One University Station, Austin, TX 78712; E-mail:
coyle@austin.utexas.edu.
Submitted for publication July 2019.
Accepted for publication March 2020.
0195-9131/20/5210-2262/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE
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Copyright © 2020 by the American College of Sports Medicine
DOI: 10.1249/MSS.0000000000002367
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II muscle fibers are activated, and when the duration is very
short (i.e., 4 s), there is little fatigue, thus allowing multiple
sprints to be performed with 30- to 45-s rest in between sprints.
This study sought to determine if very brief (4-s) cycling
performed at maximal intensity in blocks of five repetitions
per hour is effective in counteracting the effects of prolonged
sitting on postprandial lipid metabolism. In the control trial,
subjects sat for 8 h and postprandial metabolism was measured
the next day (SIT). This was compared with an exercise trial of
repeated (5) cycling sprints lasting only 4 s each, performed
every hour for 8 h (SPRINTS). Sprints were performed on an
inertial load ergometer (ILE) (14). Therefore, each hour, only
20 s of sprint exercise was performed and only 160 s of
SPRINTS was performed for the entire day.
METHODS
Subjects. Eight healthy, untrained to recreationally active
men (n= 4) and women (n= 4) were recruited to participate in
this study. Subject characteristics can be seen in Table 1. Sub-
jects were given written and verbaldescription of all the proce-
dures and measurements used in this study, and written
informed consent was obtained. The institutional review board
of the University of Texas at Austin approved this study
(ClinicalTrials.gov Identifier: NCT03856606).
Research protocol. All subjects completed two trials in
a randomized crossover design, with each trial occurring over
4 d with a minimum of 7 d between trials (Fig. 1). The first 2 d
of each trial served as a control period allowing for familiari-
zation and the control of physical activity and calorie con-
sumption before the intervention. After each control period,
subjects then performed one of the interventions on day 3.
The interventions consisted of either 8 h of prolonged sitting
(SIT) or 8 h of sitting interrupted every hour by five sprints
lasting 4 s each using the ILE (SPRINTS). The sitting time
of the trials was not different. The sprint on the ILE involves
accelerating a flywheel with a known inertia from zero
TABLE 1. Subject characteristics (n=8;4menand4women).
Characteristic Mean ± SEM Male (n=4) Female(n=4)
Age (yr) 24.0 ± 1.8 26.0 ± 2.4 22.0 ± 2.1
Height (cm) 169.0 ± 4.6 176.8 ± 6.1 161.1 ± 2.6
Body mass (kg) 70.9 ± 6.0 81.3 ± 8.0 60.4 ± 3.1
BMI (kg·m
−2
) 24.5 ± 0.8 25.8 ± 1.0 23.2 ± 0.6
RMR (kcal·d
−1
) 1727 ± 210 20,367 ± 329 1418 ± 95
FIGURE 1—Representation of experimental design. During SIT trial, subjects remained seated for 8 h, only getting up for the restroom and to prepare
food. For the SPRINTS trial, subjects spent the same time seated, only getting up for the restroom and food. However, at the end of each hour, they per-
formed five maximal sprints lasting 4 s in duration using the ILE (SPRINTS).
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velocity to the highest RPM possible in approximately 4 s.
Power per revolution of the cycle is calculated as the product
of flywheel inertia and gearing, acceleration, and velocity (14).
Controlled activity phase. During the 2-d controlled ac-
tivity phase, subjects were asked to arrive at the laboratory at
approximately 0900 h. Subjects were instructed to take be-
tween 5000 and 7500 steps per day, which is approximately
equal to a nonsedentary, low physical activity step count (15).
Subjects were then equipped with an activPAL activity moni-
tor (activPAL, PAL Technologies, Glasgow, Scotland) to be
secured onto a thigh for the assessment of body position and
movement. Steps taken were not visible to the subjects,
whereas the device was being worn; therefore, subjects were
also asked to download a pedometer application on their
mobile phones to provide visual feedback for daily step
count. Subjects were also asked to refrain from exercise
and to record all food intake and to minimize physical activ-
ity. They were then asked to repeat this diet and activity for
the remaining trial.
Intervention phase. During the SIT trial, subjects re-
mained seated for 8 h with the ability to get up for food and
restroom usage. Estimates of the caloric intake were determined
from preliminary tests of resting metabolic rate (RMR) and the
addition of approximately 20% for the energy needed for the re-
spective daily activity and maintenance of a stable body weight.
Adherence to these guidelines was checked against the pedome-
ter and activPAL, and food journals were analyzed to ensure par-
ticipants duplicated their diet for the duration of the two trials.
During the SPRINTS trial, subjects were asked to report to
the laboratory at 0900 h to begin the 8-h prolonged sit,
interrupted by ILE sprints. During the prolonged sit and during
the final 4 min of each hour, subjects performed five 4-s
sprints separated by 45 s of rest, equating to 20 s of exercise
per hour and 160 s of total time exercising on the SPRINT
day. Given that each set of five SPRINTS required approxi-
mately 5 min to complete when resting for 45 s between
SPRINTS and the fact that eight sets were completed, the total
daily time required was 40 min. During the rest periods be-
tween sprints, subjects were seated. RPE was taken after five
sprints using the standard Borg Scale (6–20). Food was pro-
vided at two times (lunch and dinner) over the duration of
the trial, and the caloric content of these meals was such that
energy balance was maintained.
High-fat/glucose tolerance test phase. The morning
after each intervention day, subjects were asked to arrive to the
laboratory to begin the high-fat/glucose tolerance test (HFGTT).
Subjects remained seated for the 6-h duration of the test except
for restroom usage. After a 5-min acclimatization period, a fasted
blood sample was obtained via antecubital venous puncture into
a 4-mL K2 EDTA vacutainer (BD Vacutainer; Fischer Scien-
tific, Hampton, NH), and plasma was subsequently aliquoted
into a microcentrifuge tube, labeled, and stored at −80°C for
future batch analysis. This process was repeated for blood
samples obtained 2, 4, and 6 h postprandially.
Subjects were asked to ingest a high-fat and carbohydrate
shake, afterwhich blood was sampled as described previously.
Atapproximately0,2,4,and6hpostprandially,expiredgas-
seswereobtainedfromeachsubject,astheywereaskedto
breathe into a meteorological balloon for a total of 15 min to
monitor fat oxidation and metabolic rate. Subject body mass
was taken by a digital scale (Ohaus, CW-11, Parsippany, NJ)
and recorded to the nearest 0.5 kg, and height was measured
using a standard stadiometer.
Blood sampling and analysis. After the collection into
K2 EDTA tubes, blood was subsequently centrifuged at
3000 rpm at 4°C for 10 min. Plasma was then aliquoted and
frozen at −80°C and later analyzed for triglyceride, glucose,
and insulin concentrations. Triglyceride was measured using
a spectrophotometric method from commercially available
kits (Pointe Scientific, Inc., Canton, MI). Glucose was mea-
sured using a similar protocol from commercially available
kits (Pointe Scientific). Plasma insulin was measured using a
microplate reader and commercially available kits (LDN Im-
munoassays and Services, Nordhorn, Germany). Coefficients
of variation for triglyceride, glucose, and insulin were 3.0%,
3.5%, and 4.9% respectively.
Diet control. The caloric content was roughly ~20%
higher than each subject’s RMR, as measured during prelimi-
nary testing. Additional energy expenditure from exercise in
the SPRINTS was estimated via indirect calorimetry. The
postexercise meals were approximately 60% carbohydrate,
20% fat, and 20% protein. For the HFGTT, subjects were pro-
vided with a high-fat shake consisting of parts melted ice
cream and heavy whipping cream, creating a macronutrient
and caloric profile of 1.34 g·kg
−1
fat, 0.92 g·kg
−1
carbohy-
drate, 0.19 g·kg
−1
protein, and 16.5 kcal·kg
−1
.
RMR and indirect calorimetry. All metabolic gas mea-
surements were made using meteorological balloons. To de-
termine RMR, subjects rested in a seated position for 15 min,
followed by a 15-min period of gas collection. Subjects
breathed through a one-way valve (Hans Rudolph, Kansas
City, MO) directly attached to a meteorological balloon. A
sample was then analyzed for concentrations of O
2
,CO
2
,
and N
2
by mass spectrometry (PerkinElmer MGA 1100, St.
Louis, MI). Gas volume was then measured via spirometry
(Vacumed, Ventura, CA). During each HFGTT, gas samples
were analyzed following the procedures detailed previously
at 0, 2, 4, and 6 h after shake ingestion for calculation of fat
and carbohydrate oxidation rate, using the tables of Frayn (16).
Statistical analysis. Incremental (AUC
I
) and total area
under the curve (AUC
T
) for concentrations of plasma triglyc-
eride, insulin, and glucose were calculated. Once calculated,
Student t-test with Bonferroni correction was used to test for
differences. Plasma insulin, glucose, and triglyceride concen-
trations were analyzed using repeated-measures two-way
ANOVA (trial–time). Likewise, daily step count and hourly
distribution of posture were analyzed using repeated-
measures two-way ANOVAs. Lastly, fasting and postprandial
RER, as well as fat and carbohydrate oxidation, were analyzed
using a repeated-measure two-way ANOVA. When interac-
tions were significant, Tukey honest significant difference
post hoc tests were run. Effect sizes were calculated as mean
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differences divided by the pooled SD (Cohen d); quantitative
criteria for effect sizes used to explain practical significance of
the findings were taken from Cohen (17). With eight partici-
pants, the study had 68% power to detect a difference of 1.0
SD (i.e., Cohen d= 1.0) between conditions.
All data were analyzed using GraphPad Prism 7 (GraphPad
Software Inc., La Jolla, CA). All data are expressed as
mean ± SEM; unless otherwise noted, the level for statistical
significance was set at P<0.05.
RESULTS
Daily steps and body posture. No significant differ-
ences were found comparing trials in daily steps, for C1, C2,
or the intervention day (Table 2). The average number of steps
taken on the intervention day was low (i.e., 3577 ± 953 and
2540 ± 969 for SPRINTS and SIT), respectively (P=0.34).
There were no significant differences between the groups for
time spent sitting (P= 0.81) or time spent standing (P=0.86).
Furthermore, the caloric intake on the intervention day was sim-
ilar for SPRINTS and SIT (2065 ± 235 and 2068 ± 232 kcal),
respectively (P=0.66).
Response to inertial load ergometry. During the
SPRINTS trial, the average power generated by the 4-s sprints
was 870 ± 139 W (male, 1107 ± 447 W; female, 632 ± 90 W)
and RPE remained low (10.0 ± 0.7; very to fairly light).
Plasma triglyceride glucose and insulin responses.
Postprandial plasma triglyceride responses are shown in
Figure 2. There was a 31% reduction in incremental AUC
I
dur-
ing the 6-h period in SPRINTS as compared with the SIT trial
(408 ± 119 vs 593 ± 88 mg·dL
−1
;P=0.009;Fig.2;Table3)
and a medium effect size (d= 0.632). However, total AUC
T
for plasma triglyceride did not reach significance between trials
(SPRINTS: 858 ± 154 mg·dL
−1
vs SIT: 1003 ± 136 mg·dL
−1
;
P= 0.11; Table 3). There were no significant differences be-
tween trials in the postprandial plasma glucose total AUC
T
(SPRINTS: 678 ± 49 mg·dL
−1
vs SIT: 707 ± 32 mg·dL
−1
;
P= 0.66) or incremental AUC
I
(SPRINTS: 150 ± 36 mg·dL
−1
vs
SIT: 159 ± 28 mg·dL
−1
;P= 0.88; Fig. 2; Table 3). Further-
more, there were no differences in insulin responses between
trials in total AUC
T
(SPRINTS: 157 ± 16 μIU·mL
−1
vs SIT:
159 ± 12 μIU·mL
−1
;P= 0.92) or incremental AUC
I
(SPRINTS: 85 ± 10 μIU·mL
−1
vs SIT: 73 ± 11 μIU·mL
−1
;
P= 0.46; Fig. 2; Table 3).
Postprandial substrate oxidation. RER demonstrated
both a significant trial effect (P= 0.001) and main effect of
time (P= 0.02) but no interaction between the two, and exhib-
ited a large effect size (d= 1.16 ± 0.04; Table 4). The average
grams of fat oxidized over the 6-h period of the HFGTT was
43% higher (P< 0.001) during SPRINTS versus SIT (SPRINTS:
TABLE 2. Daily step count and hours per day spent sitting/supine and standing in SIT or
SPRINT.
Trial
Day of Trial
Control Day 1 Control Day 2 Intervention Day
Daily Steps (steps per day)
SIT 6889 ± 1249 6626 ± 1111 2540 ± 969
a
SPRINTS 7249 ± 1264 6537 ± 1198 3577 ± 954
a
Distribution of posture (h·d
−1
)
Sitting/Supine
SIT 12.6 ± 0.7 12.7 ± 0.8 15.2 ± 0.5
a
SPRINT 12.7±1.1 12.7±0.8 14.9±0.4
Standing
SIT 2.7±0.5 2.7±0.6 0.8±0.2
a
SPRINTS 2.8±0.8 3.2±0.5 1.0±0.2
a
The controldays represent normal physical activity, and on the intervention day, sitting time
was increased and steps per day were reduced.
a
Significantly different from control days by design.
FIGURE 2—Postprandial plasma responses during the HFGTT. Plasma
triglyceride concentration (A), plasma glucose concentration (B), and
plasma insulin concentration (C).
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48.9 ± 17.7 g vs SIT: 34.1 ± 18.2 g; Table 4). Conversely, car-
bohydrate oxidation was significantly lower (P=0.002)in
SPRINTS versus SIT (SPRINTS: 13.0 ± 10.2 g vs SIT:
44.2 ± 22.3 g; Table 4).
DISCUSSION
This study reports the effects of interrupting prolonged sit-
ting with brief (4-s) maximal intensity cycling sprints on post-
prandial fat and carbohydrate metabolism measured the
following day. This investigation’s major finding was that
hourly maximal intensity 4-s sprints (performed five times
per hour) on an ILE (SPRINTS) while sitting for 8-h reduced
the next day’s postprandial plasma triglyceride incremental
AUC by 31% (P= 0.009) compared with sitting for 8 continuous
hours (SIT). Furthermore, SPRINTS significantly (P= 0.001) el-
evated fat oxidation by an average of 43% over the duration of
HFGTT corresponding to a large effect size increase compared
with SIT. This investigation did not use techniques that might
determine if the two phenomena are causally related, yet it is
possible that the postprandial lowering of plasma triglyceride
concentration was due to increased tissue uptake and oxida-
tion of the ingested plasma triglycerides.
When subjectswho are physicallyactive and taking approx-
imately >8000 steps per day add a 1-h bout of running or a ses-
sion of high-intensity interval training to their regime, they
show an improvement in their next day’s postprandial plasma
triglyceride response as well as increased fat oxidation
(18–20). This can be considered the healthy “exercise re-
sponse.”However, in people who are largely sedentary (i.e.,
2000–4000 steps per day) (15), a 1-h bout of running does
notimprovethenextday’s postprandial plasma triglyceride
response or fat oxidation (7,8). This has been termed exer-
cise resistance, as it seems that some aspect of the prolonged
inactivity is preventing the acute bout of exercise from caus-
ing healthy adaptations in fat metabolism (7,8). In the pres-
entstudy,ontheinterventiondays,thesubjectsinbothtrials
were taking <4000 steps per day and thus sedentary, outside
of the 160 s of exercise in SPRINTS. It is likely that the
hourly sprints prevented exercise resistance from occurring
and that is the reason for the enhanced fat metabolism in
SPRINTS compared with SIT. The time course with which
exercise resistance occurs from inactivity is unknown, but it
seems that the present 20 s of hourly intermittent sprints,
performed maximally in five bouts of 4 s each, was effective
in counteracting it.
The hourly set of five sprints lasting 4 s each, with 45 s of
rest, describes an exercise that is predominantly anaerobic, re-
lying heavily on stores of ATP and PC for energy during exer-
cise and oxidative metabolism for resynthesis of these stores
during recovery (21). Given that the sprints elicited maximal
power and involved maximal acceleration to an RPM of
120–160, the recruitment of both type I and type II muscle
fibers should have reached maximal levels. It is likely that
some aspect of high motor unit recruitment producing very
high anaerobic power was responsible for the effectiveness
of SPRINTS for enhancing fat metabolism (7,8). This is sur-
prising in that fat oxidation is aerobic and it might be thought
that aerobic exercise would be its specific stimulator. What
seems to be truly different about the SPRINTS exercise is
the high average maximal power (870 ± 139 W) and assumed
type II fiber recruitment. Furthermore, perceived exertion was
“very to fairly light”(10.0 ± 0.7) because of the only 4-s dura-
tion of each sprint and relatively long recovery period (45 s).
Overall, the maximal intensity sprints of 4-s duration are a rel-
atively nonfatiguing method of activating a large quantity of
muscle, and it seems that fat oxidation is improved on the fol-
lowing day.
It is not clear why the present investigation observed an
amelioration of postprandial lipemia when others, who also
broke up prolonged sitting, did not (10,11). However,
TABLE 3. Mean ± SE values for postprandial AUC responses over the 6-h postprandial
period.
Variable
Trial
SIT SPRINTS
Incremental AUC
I
Triglyceride (mg·dL
−1
6h) 593±88 408±119
a
Glucose (mg·dL
−1
6h) 159±81 150±103
Insulin (μIU·mL
−1
6 h) 72.7 ± 31 84.9 ± 28
Total AUC
T
Triglyceride (mg·dL
−1
6 h) 1003 ± 136 858 ± 154
Glucose (mg·dL
−1
6h) 707±91 678±140
Insulin (μIU·mL
−1
6h) 159±33 157±46
a
SPRINTS significantly lower than SIT (P<0.009).
TABLE 4. Postprandial substrate oxidation in SIT vs SPRINT over the 6-h period.
Hours Postprandial
Trial
SIT SPRINTS
RER (V
˙
CO
2
·V
˙
O
2
−1
)
Hour 0 0.841 ± 0.034 0.752 ± 0.014*
Hour 2 0.839 ± 0.033 0.750 ± 0.018*
Hour 4 0.823 ± 0.044 0.725 ± 0.017*
Hour 6 0.761 ± 0.022 0.709 ± 0.010
Substrate oxidation (%)
Fat
Hour 0 52.8 ± 11.1 83.1 ± 4.7**
Hour 2 53.5 ± 11.4 84.2 ± 6.0**
Hour 4 60.3 ± 14.3 90.9 ± 5.2**
Hour 6 79.1 ± 6.94 95.8 ± 3.0
Carbohydrate
Hour 0 47.3 ± 11.1 16.9 ± 4.7*
Hour 2 46.5 ± 11.4 15.9 ± 6.0*
Hour 4 39.8 ± 14.3 9.1 ± 5.2*
Hour 6 20.9 ± 6.94 4.2 ± 3.0
Substrate oxidation (g·min
−1
)
Fat
Hour 0 0.066 ± 0.016 0.122 ± 0.019**
Hour 2 0.075 ± 0.018 0.119 ± 0.016**
Hour 4 0.102 ± 0.028 0.148 ± 0.022**
Hour 6 0.136 ± 0.023 0.155 ± 0.019
Carbohydrate
Hour 0 0.145 ± 0.051 0.038 ± 0.018*
Hour 2 0.182 ± 0.055 0.055 ± 0.021*
Hour 4 0.107 ± 0.027 0.027 ± 0.017*
Hour 6 0.057 ± 0.018 0.011 ± 0.008
Energy expenditure (kcal·min
−1
)
Hour 0 1.19 ± 0.136 1.31 ± 0.168
Hour 2 1.47 ± 0.191 1.35 ± 0.184
Hour 4 1.40 ± 0.165 1.42 ± 0.179
Hour 6 1.49 ± 0.131 1.32 ± 0.127
*SPRINTS different from SIT (P< 0.05).
**SPRINTS different from SIT (P<0.01).
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improvements in glucose and insulin metabolism have been
typically seen on the day of the intervention and during the
postprandial test, yet the improvement in postprandial lipemia
has been observed the following day (12), which agrees with
our present observations. Although this study did not directly
investigate possible mechanisms, one hypothesis stems from
the dysregulation of lipoprotein lipase (LPL), the rate-
limiting enzyme for chylomicron and VLDL tissue uptake
(22,23). Indeed, prolonged inactivity has been shown to de-
crease LPL activity up to 90% and influence the amount of
heparin releasable LPL (24,25). The primary mechanism be-
hind an attenuation of postprandial lipemia is hypothesized
to be an upregulation of LPL after exercise. LPL activity typ-
ically peaks ≥8 h after exercise (26–28). Thus, it is feasible that
the periodic interruption of sitting and a large amount of mus-
cle fiber activation with SPRINTS prevented a decrease in
LPL activity during the 8-h period of sitting used by this inves-
tigation. It is noteworthy that this might be achieved with only
20 s·h
−1
of exercise, albeit at maximal power.
Previous research has shown that aerobic exercise at 30%–
70% of V
˙
O
2max
with a minimum of ~360–950 kcal of energy
expenditure is needed to reduce postprandial lipemia the next
day (18,19,29–32). In the present study, participants expended
much less energy with an amount that is below the health
guidelines recommended for energy expenditure (33). How-
ever, a reduction in postprandial lipemia from small amounts
of energy expenditure is not unprecedented, as resistance exer-
cise as well as sprint interval cycling, without caloric replace-
ment, has been shown to cause postprandial lipemia reduction
(34–36). The low energy expenditure and low time commit-
ment could be seen as a benefit to SPRINTS type exercise per-
formed for only 4 s, and five times per hour, because the main
reason people give for not exercising is lack of time (9). How-
ever, over the eight sets of hourly sprints of the present design,
the total time involvement amounted to 40 min, which could
be reduced by shortening the recovery period between sprints
or by reducing the number of sets. Using similar test meals and
design, we have shown significant reductions in integrated tri-
glyceride AUC
I
with 1-h bouts of treadmill running, or cycling
at intensities ranging from 50% to 90% V
˙
O
2max
(19,20). Kim
et al. (19) found a 27% reduction in the AUC
I
after running at
65% V
˙
O
2max
for 1 h. Similar reductions in triglyceride AUC
I
(i.e., 31%) were seen in the present study with a total exercise
time of only 160 s (2.7 min). The most salient aspect of the ex-
ercise bouts were that each 4-s sprint was performed at true
maximal power output, which in these subjects averaged 870 W.
This maximal power is roughly three to four times the power
needed to elicit maximal oxygen uptake. Indeed, the 4-s sprints,
by eliciting maximal power output, represent the highest possi-
ble rate of muscle fiber recruitment, especially of type II muscle
fibers but without fatigue. This is unlike cycling sprints that last
for 20–30-s durations and elicit an extreme accumulation of lac-
tic acid and intense fatigue (37).
The negative health consequences of prolonged sitting and
inactivity are often lumped together because most of the pe-
riods in which people are inactive; they spend sitting and
sometimes standing (38). As a result, it could be thought that
the act of sitting per se is unhealthy compared with other forms
of inactivity. In the present study, the sitting time was the same
in SIT and SPRINTS, given that so little time was spent
exercising in SPRINTS and the recovery time was spent
seated. Our observation that the next day’s postprandial hyper-
lipemia after 8 h of sitting could be successfully overcome by
physical activity that amounted to only 160 s indicates that sit-
ting may not be inherently negative beyond its inactivity, at
least in terms of postprandial lipemia.
Although the present study adds to the body of literature re-
garding inactivity and postprandial responses, it is not without
limitations. We did not control for phase of menstrual cycle in
the female participants, as it has been previously shown that
postprandial responses vary according to phase of menstrual
cycle (39). This may have influenced the study findings. Fur-
thermore, this study made use of a small number of subjects re-
ducing the statistical power and increasing the likelihood of
type II errors, as such potential differences between trials
may not be fully represented. This also extends to the ability
to detect sex differences within the study design. A previous
quantitative review has suggested that sex may play a role in
acute exercise-induced reductions of postprandial lipemia
(18). In that review, sex was found to be a moderator with
the effect size of the postexercise reductions being larger in fe-
males when compared with males (18). Lastly, this study in-
vestigated a young, lean, and apparently healthy population.
Even within the SIT trial, subjects displayed favorable re-
sponses. It is unclear if SPRINT exercise might improve me-
tabolism in those with a less than favorable metabolic
profile. It might also depend on their level of background
physical activity as reflected in their step count per day (7).
Furthermore, mechanistic theorizing is beyond the scope of
this study, as it was not designed to determine a mechanism
as to how SPRINTS affect postprandial responses, rather if
such a low volume of exercise could provide an impact.
In conclusion, these data indicate that hourly, maximal ef-
fort, 4-s sprints on an ILE, which interrupts prolonged sitting,
lowers postprandial incremental plasma triglyceride concen-
tration by 31% (P= 0.009) and simultaneously increases fat
oxidation by an average of 43% (P< 0.001) during the next
day. This is particularly significant when considering the small
amount of energy expended, the low RPE reported by the sub-
jects, and the minimal amount of time spent exercising
(160 sd
−1
). The brief nature and nonfatiguing aspect of the ex-
ercise might lead to better adherence when compared with cur-
rent exercise recommendations (6). The clinical significance
of these findings is centered on reductions in postprandial tri-
glyceride incremental AUC and increased fat oxidation, which
likely lead to improved cardiometabolic health.
We thank the subjects for their participation. As a matter of financial
interest disclosure, E. F. Coyle owns equity in Sports Texas Nutri-
tion Training and Fitness, Inc., a company that sells the inertial
load ergometer used in this study. The results of this study do
not constitute endorsement by the American College of Sports
Medicine.
INERTIAL LOAD ERGOMETRY IMPROVES FAT METABOLISM Medicine & Science in Sports & Exercise
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2267
APPLIED SCIENCES
Copyright © 2020 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
A. S. W. and E. F. C. conceived the research and designed the experi-
ment;A.S.W.,H.M.B.,andE.V.recruitedsubjectsandperformedexper-
iments;A.S.W.andE.F.C.interpretedresultsofexperiments;A.S.W.
prep ared fig ures, performed statistical analyses, and drafted the manuscript;
A. S. W., H. M. B., E. V., and E. F.C. edited and revised the manuscript;
A. S. W., H. M. B., E. V., and E. F. C. approved the final version of the manuscript.
The results are presented clearly, honestly, and without fabrication,
falsification, or inappropriate data manipulation.
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