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Hourly 4-s Sprints Prevent Impairment of Postprandial Fat Metabolism from Inactivity

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High postprandial plasma lipids (PPL; i.e., triglycerides) are a risk factor for cardiovascular disease. Physical inactivity, characterized by prolonged sitting 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 × 5 per hour × 8 h = 160 s·d 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 per 6 h; P = 0.009) decrease in plasma triglyceride incremental AUC and a 43% increase in whole-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 young adults. Given that these improvements were elicited from 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 metabolism and other aspects of health.
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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. 22622269, 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 days 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 timeand reduced the need to move
(13). 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 (24).
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
(24). A large epidemiological study (3), estimated that in
order to counteract the effects of prolonged sitting, a person
needs to exercise for 6075 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
13 min every 1530 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 (1012).
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 1224 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
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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 1Representation 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 (620). 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 subjects 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 (trialtime). 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 2Postprandial 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 investigations 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 days 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 days postprandial plasma
triglyceride response as well as increased fat oxidation
(1820). This can be considered the healthy exercise re-
sponse.However, in people who are largely sedentary (i.e.,
20004000 steps per day) (15), a 1-h bout of running does
notimprovethenextdays 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
120160, 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 (2628). 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 ~360950 kcal of energy
expenditure is needed to reduce postprandial lipemia the next
day (18,19,2932). 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
(3436). 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 2030-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 days 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
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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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... The only condition or exercise that seems to "break through" the exercise resistance of subjects taking only less than 4000 steps·d −1 was the interruption of prolonged sitting with hourly maximal "all-out" intensity cycling sprints of only 4-s duration (see below). In those cases, the brief hourly cycling sprints (5 Â 4-s) were begun in the morning and continued until the evening (36). This suggests that the timing of exercise is important for offsetting exercise resistance and that the volume does not have to be large. . ...
... We next determined if the interruption of prolonged sitting (i.e., 8 h of inactivity) with hourly maximal all-out intensity cycling sprints of only 4-s duration each (i.e., 5  4-s sprints per hour  8 h = 160 s·d −1 or 2.7 min·d −1 of "sprints") improve and normalize the PPTG response and fat oxidation (36). The 4-s sprints used an inertial load ergometer and were followed by 45 s of seated rest (36). ...
... We next determined if the interruption of prolonged sitting (i.e., 8 h of inactivity) with hourly maximal all-out intensity cycling sprints of only 4-s duration each (i.e., 5  4-s sprints per hour  8 h = 160 s·d −1 or 2.7 min·d −1 of "sprints") improve and normalize the PPTG response and fat oxidation (36). The 4-s sprints used an inertial load ergometer and were followed by 45 s of seated rest (36). People usually state that a major reason for not being physically active or exercising is lack of time (37). ...
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Prolonged sitting prevents a 1-h bout of running from improving fat oxidation and reducing plasma triglycerides. This "Exercise Resistance" can be prevented by taking 8,500 steps/d or by interrupting 8-h of sitting with hourly cycle sprints. We hypothesize that there is an interplay between background physical activity (e.g.; steps/d) and the exercise stimuli in regulating some acute and chronic adaptations to exercise.
... High-intensity interval training also reduces time in a session compared with continuous training (12,13). We recently reported that hourly bouts of acute 4 s of maximal intensity cycle sprints that interrupt prolonged sitting can significantly lower the next day's postprandial plasma triglyceride response while increasing fat oxidation (14). The present study extends those acute observations of the effects of 4-s maximal intensity bouts to 8 wk of training. ...
... We suspect that increases in leg muscle mass contributed significantly (41), but presently have no direct data. We have previously shown that these repeated 4-s sprints performed hourly in blocks of five throughout the day, stimulate reductions in postprandial plasma triglycerides, as well as increased fat oxidation (14). However, we did not measure fat metabolism in the present study to identify a potential training response. ...
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... This may be an explanation that why the fat oxidation cannot be further increased after consuming a high fat meal. Nonetheless, this present study indicated that time-restricted feeding increased the fasting and postprandial fat oxidation, which likely lead to improved fat metabolism or cardiometabolic health 28 . Moreover, the further research is required to investigate the effect of TRF on postprandial response after a high fat meal in the overweight or at-risk populations. ...
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Studies have revealed that time-restricted feeding affects the fat oxidation rate; however, its effects on the fat oxidation rate and hyperlipidemia following high-fat meals are unclear. This study investigated the effects of 5-day time-restricted feeding on the fat oxidation rate and postprandial lipemia following high fat meals. In this random crossover experimental study, eight healthy male adults were included each in the 5-day time-restricted feeding trial and the control trial. The meals of the time-restricted feeding trial were provided at 12:00, 16:00, and 20:00. The meals of the control trial were provided at 08:00, 14:00, and 20:00. The contents of the meals of both trials were the same, and the calories of the meals met the 24-h energy requirement of the participants. After 5 days of the intervention, the participants consumed high-fat meals on the sixth day, and their physiological changes were determined. The fasting fat oxidation rate ( p < 0.001) and postprandial fat oxidation rate ( p = 0.019) of the time-restricted feeding trial were significantly higher than those of the control trial. The 24-h energy consumption and postprandial triglyceride, blood glucose, insulin, glycerol, and free fatty acid concentrations of the two trials showed no significant differences ( p > 0.05). The results revealed that 5 days of time-restricted feeding effectively increased the fasting and postprandial fat oxidation rate, but it did not affect postprandial lipemia.
... Despite the known reductions in the proportion of type 1 muscle fibers (34)(35)(36)(37)(38) and capacity to increase exercise energy expenditure (39) with SCI, the rates of FO of our participants in the postabsorptive resting (0.08 ± 0.02 g/min) and postprandial states (0.10 ± 0.03 g/min) are very similar to those of non-injured participants (0.06-0.08 and 0.08-0.12 g/min, respectively) (14,33,40,41). ...
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... Previous studies suggest that avoiding exercise resistance may occur with as little as~7900 steps per day (4). We have recently observed that if prolonged sitting throughout the day is interrupted hourly by 20 s of maximal cycling (5 Â 4-s bouts), exercise resistance can be prevented at least in terms of fat metabolism (39). It thus seems that exercise resistance can be prevented not just by accumulating steps throughout the day but also by accumulating bouts of very short maximal-intensity exercise. ...
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Since ancient times, the health benefits of regular physical activity/exercise have been recognised and the classic studies of Morris and Paffenbarger provided the epidemiological evidence in support of such an association. Cardiorespiratory fitness, often measured by maximal oxygen uptake, and habitual physical activity levels are inversely related to mortality. Thus, studies exploring the biological bases of the health benefits of exercise have largely focused on the cardiovascular system and skeletal muscle (mass and metabolism), although there is increasing evidence that multiple tissues and organ systems are influenced by regular exercise. Communication between contracting skeletal muscle and multiple organs has been implicated in exercise benefits, as indeed has other inter-organ "cross-talk". The application of molecular biology techniques and 'omics' approaches to questions in exercise biology has opened new lines of investigation to better understand the beneficial effects of exercise and, in so doing, inform the optimisation of exercise regimens and the identification of novel therapeutic strategies to enhance health and well-being.
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High levels of sedentary time and physical inactivity independently contribute to the development of noncommunicable diseases and premature mortality. Engaging in at least 150 min of moderate or 75 min of vigorous physical activity (PA) is globally recognized as conferring substantial health benefits. However, setting these distinct thresholds and promoting them may have inadvertently created perceptions among the general public that an all or nothing phenomenon exists. Yet, the PA guidelines and a growing body of evidence highlights the robust health benefits associated with becoming more active from a previously sedentary lifestyle, even if the volume of PA performed is below current ideal recommendations. Practitioners providing PA recommendations are encouraged to initially highlight the benefits of moving more and sitting less rather than initially setting lofty, perhaps unachievable, PA goals for inactive individuals. Taking this approach may increase the likelihood of adopting a more physically active lifestyle and ultimately progressing to meet the PA guidelines.
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The interaction of prolonged sitting with physical exercise for maintaining health is unclear. We tested the hypothesis that prolonged siting would have a deleterious effect on postprandial plasma lipemia (PPL, postprandial plasma triglycerides) and abolish the ability of an acute exercise bout to attenuate PPL. Seven healthy young men performed three interventions over 5 days (D1-5) in a randomized crossover design with > 1 week between interventions: 1) sitting >14h/d with hypercaloric energy balance (SH), 2) sitting >14h/d with net energy balance (SB), and 3) active walking/standing with net energy balance (WB) and sitting 8.4 h/d. The first high fat tolerance test (HFTT1) was performed on D3 following 2 days of respective interventions. On the evening of D4 subjects ran on a treadmill for 1-h at ~ 67% VO2max, followed by the second HFTT (HFTT2) on D5. Two days of prolonged sitting increased TG AUCI (i.e., incremental area under the curve for TG), irrespective of energy balance, compared to WB (27% in SH, p=0.003 and 26% in SB, p=0.046). Surprisingly, after four days of prolonged sitting (i.e.; SH and SB), the acute exercise on D4 failed to attenuate TG AUCI or increase relative fat oxidation in HFTT2, compared to HFTT1, independent of energy balance. In conclusion, prolonged sitting over several days was sufficient to amplify PPL and to abolish the beneficial effect of acute exercise on lowering PPL and raising fat oxidation, regardless of energy balance. This underscores the importance of limiting sitting time even in people who have exercised.
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Sedentary behavior is highly prevalent in office-based workplaces; however, few studies have assessed the attributes associated with this health risk factor in the workplace setting. This study aimed to identify the correlates of office workers' objectively-assessed total and prolonged (≥ 30 min bouts) workplace sitting time. Participants were 231 Australian office workers recruited from 14 sites of a single government employer in 2012–13. Potential socio-demographic, work-related, health-related and cognitive-social correlates were measured through a self-administered survey and anthropometric measurements. Associations with total and prolonged workplace sitting time (measured with the activPAL3) were tested using linear mixed models. Worksites varied significantly in total workplace sitting time (overall mean [SD]: 79% [10%] of work hours) and prolonged workplace sitting time (42% [19%]), after adjusting for socio-demographic and work-related characteristics. Organisational tenure of 3–5 years (compared to tenure > 5 years) was associated with more time spent in total and prolonged workplace sitting time, while having a BMI categorised as obese (compared to a healthy BMI) was associated with less time spent in total and prolonged workplace sitting time. Significant variations in sitting time were observed across different worksites of the same employer and the variation remained after adjusting for individual-level factors. Only BMI and organisational tenure were identified as correlates of total and prolonged workplace sitting time. Additional studies are needed to confirm the present findings across diverse organisations and occupations.
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Aim: To compare the cumulative (three-day) effect of prolonged sitting on metabolic responses during a mixed meal tolerance test (MTT), with sitting that is regularly interrupted with brief bouts of light-intensity walking. Research design and methods: Overweight/obese adults (n=19) were recruited for a randomized, three-day, outpatient, crossover trial involving: 1) 7-hour days of uninterrupted sitting (SIT); and, 2) 7-hour days of sitting with light-intensity activity breaks [BREAKS; 2-minutes of treadmill walking (3.2 km/hour) every 20 minutes (total: 17 breaks/day)]. On days 1 and 3, participants underwent a MTT (75g carbohydrate, 50g fat), and the incremental area under the curve (iAUC) was calculated from hourly blood samples. GEE models were adjusted for gender, BMI, energy intake, treatment order and pre-prandial values to determine effects of time, condition and time x condition. Results: The glucose iAUC was 1.3 ± 0.5 and 1.5 ± 0.5 mmol.hr.L-1 (mean difference ± SEM) higher in SIT compared with BREAKS on days 1 and 3 respectively (condition effect: P=0.001), with no effect of time (P=0.48) or time x condition (P=0.8). The insulin iAUC was also higher on both days in SIT (Day 1: ∆151 ± 73, Day 3: ∆91 ± 73 pmol.hr.L-1, P=0.01), with no effect of time (P=0.52) or time x condition (P=0.71). There was no between-treatment difference in triglycerides iAUC. Conclusion: There were significant between-condition effects but no temporal change in metabolic responses to MTT, indicating that breaking up sitting over three days sustains, but does not enhance, the lowering of postprandial glucose and insulin.
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Acute exercise improves postprandial lipemia, glucose tolerance, and insulin sensitivity, all of which are risk factors for cardiovascular disease. However, recent research suggests that prolonged sedentary behavior might abolish these healthy metabolic benefits. Accordingly, this study aimed to elucidate the impact of an acute bout of exercise on postprandial plasma triglyceride, glucose, and insulin concentrations after 4 days of prolonged sitting (~13.5 h/day). Ten untrained to recreationally active men ( n = 5) and women ( n = 5) completed a counterbalanced, crossover study. Four days of prolonged sitting without exercise (SIT) were compared with 4 days of prolonged sitting with a 1-h bout of treadmill exercise (SIT + EX; 63.1 ± 5.2% V̇o 2max ) on the evening of the fourth day. The following morning, participants completed a high-fat/glucose tolerance test (HFGTT), during which plasma was collected over a 6-h period and analyzed for triglycerides, glucose, and insulin. No differences between trials ( P > 0.05) were found in the overall plasma triglyceride, glucose, or insulin responses during the HFGTT. This lack of difference between trials comes with similarly low physical activity (~3,500–4,000 steps/day) on each day except for the 1-h bout of exercise during SIT + EX the day before the HFGTT. These data indicate that physical inactivity (e.g., sitting ~13.5 h/day and <4,000 steps/day) creates a condition whereby people become “resistant” to the metabolic improvements that are typically derived from an acute bout of aerobic exercise (i.e., exercise resistance). NEW & NOTEWORTHY In people who are physically inactive and sitting for a majority of the day, a 1-h bout of vigorous exercise failed to improve lipid, glucose, and insulin metabolism measured the next day. It seems that something inherent to inactivity and/or prolonged sitting makes the body resistant to the 1 h of exercise preventing the normally derived metabolic improvements following exercise.
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Importance Approximately 80% of US adults and adolescents are insufficiently active. Physical activity fosters normal growth and development and can make people feel, function, and sleep better and reduce risk of many chronic diseases. Objective To summarize key guidelines in the Physical Activity Guidelines for Americans, 2nd edition (PAG). Process and Evidence Synthesis The 2018 Physical Activity Guidelines Advisory Committee conducted a systematic review of the science supporting physical activity and health. The committee addressed 38 questions and 104 subquestions and graded the evidence based on consistency and quality of the research. Evidence graded as strong or moderate was the basis of the key guidelines. The Department of Health and Human Services (HHS) based the PAG on the 2018 Physical Activity Guidelines Advisory Committee Scientific Report. Recommendations The PAG provides information and guidance on the types and amounts of physical activity to improve a variety of health outcomes for multiple population groups. Preschool-aged children (3 through 5 years) should be physically active throughout the day to enhance growth and development. Children and adolescents aged 6 through 17 years should do 60 minutes or more of moderate-to-vigorous physical activity daily. Adults should do at least 150 minutes to 300 minutes a week of moderate-intensity, or 75 minutes to 150 minutes a week of vigorous-intensity aerobic physical activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity. They should also do muscle-strengthening activities on 2 or more days a week. Older adults should do multicomponent physical activity that includes balance training as well as aerobic and muscle-strengthening activities. Pregnant and postpartum women should do at least 150 minutes of moderate-intensity aerobic activity a week. Adults with chronic conditions or disabilities, who are able, should follow the key guidelines for adults and do both aerobic and muscle-strengthening activities. Recommendations emphasize that moving more and sitting less will benefit nearly everyone. Individuals performing the least physical activity benefit most by even modest increases in moderate-to-vigorous physical activity. Additional benefits occur with more physical activity. Both aerobic and muscle-strengthening physical activity are beneficial. Conclusions and Relevance The Physical Activity Guidelines for Americans, 2nd edition, provides information and guidance on the types and amounts of physical activity that provide substantial health benefits. Health professionals and policy makers should facilitate awareness of the guidelines and promote the health benefits of physical activity and support efforts to implement programs, practices, and policies to facilitate increased physical activity and to improve the health of the US population.
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Background Compared to prolonged sitting, regular activity breaks immediately lower postprandial glucose and insulin, but not triglyceride responses. Postprandial triglycerides can be lowered by physical activity but the effect is often delayed by ∼12-24 h Objective To determine whether regular activity breaks affect postprandial triglyceride response in a delayed manner similar to physical activity. Methods In a randomized crossover trial, 36 adults (BMI 23.9 kg·m² (SD 3.9)) completed four two-day interventions: 1. Prolonged Sitting (SIT); 2. Prolonged Sitting with 30 min of continuous walking (60% VO2max), at the end of Day 1 (SIT+PAD1); 3. Sitting with 2 min of walking (60% VO2max) every 30 min (RAB); 4. A combination of the continuous walking and regular activity breaks in 2 and 3 above (RAB+PAD1). Postprandial plasma triglyceride, non-esterified fatty acids (NEFA), glucose, and insulin responses were measured in venous blood over 5 h on Day 2. Results Compared to SIT, both RAB (difference: -43.61 mg·dL⁻¹·5h; 95% CI –83.66 to -2.67; p=0.035) and RAB+PAD1 (-65.86 mg·dL⁻¹·5h; 95% CI -112.14 to -19.58; p=0.005) attenuated triglyceride tAUC. RAB+PAD1 produced the greatest reductions in insulin tAUC (-23%; 95% CI -12 to -31%; p<0.001) while RAB resulted in the largest increase in NEFA (tAUC, 10.08 mg·dL⁻¹·5h; 95% CI 5.60 to 14.84; p<0.001). There was no effect on glucose tAUC (p=0.290). Conclusions Postprandial triglyceride response is attenuated by regular activity breaks, when measured ∼24 h after breaks begin. Combining regular activity breaks with 30 min of continuous walking further improves insulinaemic and lipidaemic responses.
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Background: High amounts of sedentary behaviour have been associated with increased risks of several chronic conditions and mortality. However, it is unclear whether physical activity attenuates or even eliminates the detrimental effects of prolonged sitting. We examined the associations of sedentary behaviour and physical activity with all-cause mortality. Methods: We did a systematic review, searching six databases (PubMed, PsycINFO, Embase, Web of Science, Sport Discus, and Scopus) from database inception until October, 2015, for prospective cohort studies that had individual level exposure and outcome data, provided data on both daily sitting or TV-viewing time and physical activity, and reported effect estimates for all-cause mortality, cardiovascular disease mortality, or breast, colon, and colorectal cancer mortality. We included data from 16 studies, of which 14 were identified through a systematic review and two were additional unpublished studies where pertinent data were available. All study data were analysed according to a harmonised protocol, which categorised reported daily sitting time and TV-viewing time into four standardised groups each, and physical activity into quartiles (in metabolic equivalent of task [MET]-hours per week). We then combined data across all studies to analyse the association of daily sitting time and physical activity with all-cause mortality, and estimated summary hazard ratios using Cox regression. We repeated these analyses using TV-viewing time instead of daily sitting time. Findings: Of the 16 studies included in the meta-analysis, 13 studies provided data on sitting time and all-cause mortality. These studies included 1 005 791 individuals who were followed up for 2-18·1 years, during which 84 609 (8·4%) died. Compared with the referent group (ie, those sitting <4 h/day and in the most active quartile [>35·5 MET-h per week]), mortality rates during follow-up were 12-59% higher in the two lowest quartiles of physical activity (from HR=1·12, 95% CI 1·08-1·16, for the second lowest quartile of physical activity [<16 MET-h per week] and sitting <4 h/day; to HR=1·59, 1·52-1·66, for the lowest quartile of physical activity [<2·5 MET-h per week] and sitting >8 h/day). Daily sitting time was not associated with increased all-cause mortality in those in the most active quartile of physical activity. Compared with the referent (<4 h of sitting per day and highest quartile of physical activity [>35·5 MET-h per week]), there was no increased risk of mortality during follow-up in those who sat for more than 8 h/day but who also reported >35·5 MET-h per week of activity (HR=1·04; 95% CI 0·99-1·10). By contrast, those who sat the least (<4 h/day) and were in the lowest activity quartile (<2·5 MET-h per week) had a significantly increased risk of dying during follow-up (HR=1·27, 95% CI 1·22-1·31). Six studies had data on TV-viewing time (N=465 450; 43 740 deaths). Watching TV for 3 h or more per day was associated with increased mortality regardless of physical activity, except in the most active quartile, where mortality was significantly increased only in people who watched TV for 5 h/day or more (HR=1·16, 1·05-1·28). Interpretation: High levels of moderate intensity physical activity (ie, about 60-75 min per day) seem to eliminate the increased risk of death associated with high sitting time. However, this high activity level attenuates, but does not eliminate the increased risk associated with high TV-viewing time. These results provide further evidence on the benefits of physical activity, particularly in societies where increasing numbers of people have to sit for long hours for work and may also inform future public health recommendations. Funding: None.
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-Nine male subjects performed two bouts of 30-s maximal isokinetic cycling. Each bout of exercise was performed at 80 revolutions/min and was separated by 4 min of recovery. Mixed-muscle phosphocreatine (: PCr resynthesis during recovery (88.1 ±6.1%) was positively correlated with the restoration of total work production during bout 2 (r = 0.80, P < 0.05). During bout 1, ATP and PCr utilization were greater in type II compared with type I fibers (P < 0.01 and P< 0.05, respectively). The subsequent 4-min period of recovery was insufficient to allow total restoration of ATP and PCr in type II fibers, but restoration of ATP and PCr in type I fibers was almost complete. During the second bout of exercise, ATP and PCr utilization were reduced in type II fibers (P < 0.01), without a corresponding change in type I fibers, and performance was also significantly reduced. The reduction in work capacity observed during bout 2 may have been related to a slower resynthesis, and consequently a reduced availability, of ATP and PCr in type II fibers.
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Objective: To encourage increased participation in physical activity among Americans of all ages by issuing a public health recommendation on the types and amounts of physical activity needed for health promotion and disease prevention. Participants: A planning committee of five scientists was established by the Centers for Disease Control and Prevention and the American College of Sports Medicine to organize a workshop. This committee selected 15 other workshop discussants on the basis of their research expertise in issues related to the health implications of physical activity. Several relevant professional or scientific organizations and federal agencies also were represented. Evidence: The panel of experts reviewed the pertinent physiological, epidemiologic, and clinical evidence, including primary research articles and recent review articles. Consensus process: Major issues related to physical activity and health were outlined, and selected members of the expert panel drafted sections of the paper from this outline. A draft manuscript was prepared by the planning committee and circulated to the full panel in advance of the 2-day workshop. During the workshop, each section of the manuscript was reviewed by the expert panel. Primary attention was given to achieving group consensus concerning the recommended types and amounts of physical activity. A concise "public health message" was developed to express the recommendations of the panel. During the ensuing months, the consensus statement was further reviewed and revised and was formally endorsed by both the Centers for Disease Control and Prevention and the American College of Sports Medicine. Conclusion: Every US adult should accumulate 30 minutes or more of moderate-intensity physical activity on most, preferably all, days of the week.