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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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... 殷明越 1 刘骞 2 李汉森 3 张博翼 4,5 杨臻 6 谭伊能 7 陈志力 1 邓盛基 1 [29][30][31][32][33][34][35][36][37][38][39][40] 、胰岛素 [41,29,31,33,35,39,40] 和血脂 [41,29,36,42,39,43,44] 。也 有研究发现,血糖 [41,42,45,46,43,47] 、胰岛素和血脂 [38,47] [16] 的回归分析显示 BMI 较高的受试者血糖改善更显著。活动水平与性别也是影响因 素之一,久坐或无训练人群可能在久坐间断出现更显著的血糖降低 [27] ,而目前性别差异在久坐间断改善 糖、脂代谢方面的试验结果并不一致 [32,36] ,尽管先前研究发现女性进行久坐间断改善血压的幅度相较于 男性更小 [80] 。此外,血糖受损(包括确诊糖尿病与糖尿病前期)人群更能从久坐间断中获得健康益处 [16] ,其对运动刺激的反应更为敏感 [53,96] 。糖、脂代谢方面可能归因于胰岛素敏感患者血糖的转运、摄取 和代谢程度更高 [97] ,而血管功能方面表现于临床人群由于更高的静息血压值导致久坐间断后更易出现血 压下降 [98] ,此前对健康人群的久坐试验 [ [65] ,Paing 等 [102] 也有类似发现。然而,也有 研究显示低频率在改善血糖 [62,67] [103,104] ,也可能是大肌肉群收缩活动唤起肝脏葡萄糖释放 [62] 。研究显示,运动间断久坐会改变骨骼肌中与 碳水化合物代谢调节相关的 10 个基因的表达 [105] ,包括动力蛋白轻链表达增加,这可能增加细胞内 GLUT4 转运至质膜的数量。其中,胰岛素介导通过"胰岛素受体-胰岛素受体底物-磷脂酰肌醇 3-激酶 -蛋白激酶 B"的途径实现 GLUT4 转运 [106] ;而骨骼肌收缩介导则与运动时能量消耗所唤起的高代谢需求 相关,涉及酶活性升高、Ca 2+ 浓度增加和底物磷酸化等 [107] 。此外,运动可急性提升脂蛋白脂肪酶活性 [108] 和促进肌动蛋白分泌 [109] ,前者能有效降解血浆中的甘油三酯,而后者能激活相关酶促使 GLUT4 转运。 久坐的低代谢需求使血管舒张代谢物相应较低,导致毛细血管口径最小化并降低与供血动脉的压 差,同时一氧化氮减少与内皮素-1(endothelin 1,ET-1) [86] 增加会导致平滑肌血管收缩从而增加外周阻力 与平均动脉压 [110] 。研究显示,5 h 持续久坐后 ET-1 显著升高,以 30 min/次进行单次 3 min 的自重抗阻间 断久坐则使得其降低 [85] 。久坐还会引起交感神经系统活性升高,使得血浆去甲肾上腺素升高引起血管收 缩导致血管外周阻力变化 [111] 影响血压。久坐间断被认为能逆转上述环节,如使血浆去甲肾上腺素水平降 低 [80] ,也可能通过骨骼肌收缩增加以诱发更强的肌肉升压反射,使运动后血管舒张加强以降低血浆去甲 肾上腺素和血压 [112] 。然而,除去激素分泌以外,仍需要更为直接的交感神经系统活动指标测量以支持这 一机制。 动作模式方面,久坐(髋、膝关节弯曲)会阻碍血流和影响剪切应力模式从而增加血管阻力,久坐 间断能够减轻这一影响。先前研究发现,受试者久坐后小腿周长的增加 [113] 进而导致静脉汇集和血流量及 切应力下降 [114] ,其表明久坐引起的血管动力学下降还可能与持续重力影响下的下肢静水压力 [115] 相关。此 外,也有研究认为血液黏稠度增加 [116] 也可能是潜在机制之一。 图 2 运动间断久坐急性影响糖、脂代谢与血管功能的改善机理 [100] 4.6 循证实践建议与未来研究方向 本研究结果可综合 Ekelund 等 [117] 对久坐或体力活动与全因死亡率的关联分析,作为久坐的健康风险 参照标准(图 3-A) ,以基于风险状况选择不同的久坐间断策略(图 3-B) 。例如:中风险人群通过较高单 次负荷量的低~中强度运动以特定频率进行间断,低风险与部分中风险人群(青壮年等)可尝试考虑通过 高强度运动 [100,101] 或低量(<5 min)高强度间歇训练 [118] 间断久坐以累积运动量 [119] ,进而促进心脏代谢健 康 [17] 与体成分改善。图 3-C 总结了递增策略每一级的训练建议,不同人群还可依据不同糖、脂代谢与血 管功能促进目标参考本研究结果与讨论部分。 图 3 风险参考矩阵与久坐间断"台阶式"递增策略 ...
... 殷明越 1 刘骞 2 李汉森 3 张博翼 4,5 杨臻 6 谭伊能 7 陈志力 1 邓盛基 1 [29][30][31][32][33][34][35][36][37][38][39][40] 、胰岛素 [41,29,31,33,35,39,40] 和血脂 [41,29,36,42,39,43,44] 。也 有研究发现,血糖 [41,42,45,46,43,47] 、胰岛素和血脂 [38,47] [16] 的回归分析显示 BMI 较高的受试者血糖改善更显著。活动水平与性别也是影响因 素之一,久坐或无训练人群可能在久坐间断出现更显著的血糖降低 [27] ,而目前性别差异在久坐间断改善 糖、脂代谢方面的试验结果并不一致 [32,36] ,尽管先前研究发现女性进行久坐间断改善血压的幅度相较于 男性更小 [80] 。此外,血糖受损(包括确诊糖尿病与糖尿病前期)人群更能从久坐间断中获得健康益处 [16] ,其对运动刺激的反应更为敏感 [53,96] 。糖、脂代谢方面可能归因于胰岛素敏感患者血糖的转运、摄取 和代谢程度更高 [97] ,而血管功能方面表现于临床人群由于更高的静息血压值导致久坐间断后更易出现血 压下降 [98] ,此前对健康人群的久坐试验 [ [65] ,Paing 等 [102] 也有类似发现。然而,也有 研究显示低频率在改善血糖 [62,67] [103,104] ,也可能是大肌肉群收缩活动唤起肝脏葡萄糖释放 [62] 。研究显示,运动间断久坐会改变骨骼肌中与 碳水化合物代谢调节相关的 10 个基因的表达 [105] ,包括动力蛋白轻链表达增加,这可能增加细胞内 GLUT4 转运至质膜的数量。其中,胰岛素介导通过"胰岛素受体-胰岛素受体底物-磷脂酰肌醇 3-激酶 -蛋白激酶 B"的途径实现 GLUT4 转运 [106] ;而骨骼肌收缩介导则与运动时能量消耗所唤起的高代谢需求 相关,涉及酶活性升高、Ca 2+ 浓度增加和底物磷酸化等 [107] 。此外,运动可急性提升脂蛋白脂肪酶活性 [108] 和促进肌动蛋白分泌 [109] ,前者能有效降解血浆中的甘油三酯,而后者能激活相关酶促使 GLUT4 转运。 久坐的低代谢需求使血管舒张代谢物相应较低,导致毛细血管口径最小化并降低与供血动脉的压 差,同时一氧化氮减少与内皮素-1(endothelin 1,ET-1) [86] 增加会导致平滑肌血管收缩从而增加外周阻力 与平均动脉压 [110] 。研究显示,5 h 持续久坐后 ET-1 显著升高,以 30 min/次进行单次 3 min 的自重抗阻间 断久坐则使得其降低 [85] 。久坐还会引起交感神经系统活性升高,使得血浆去甲肾上腺素升高引起血管收 缩导致血管外周阻力变化 [111] 影响血压。久坐间断被认为能逆转上述环节,如使血浆去甲肾上腺素水平降 低 [80] ,也可能通过骨骼肌收缩增加以诱发更强的肌肉升压反射,使运动后血管舒张加强以降低血浆去甲 肾上腺素和血压 [112] 。然而,除去激素分泌以外,仍需要更为直接的交感神经系统活动指标测量以支持这 一机制。 动作模式方面,久坐(髋、膝关节弯曲)会阻碍血流和影响剪切应力模式从而增加血管阻力,久坐 间断能够减轻这一影响。先前研究发现,受试者久坐后小腿周长的增加 [113] 进而导致静脉汇集和血流量及 切应力下降 [114] ,其表明久坐引起的血管动力学下降还可能与持续重力影响下的下肢静水压力 [115] 相关。此 外,也有研究认为血液黏稠度增加 [116] 也可能是潜在机制之一。 图 2 运动间断久坐急性影响糖、脂代谢与血管功能的改善机理 [100] 4.6 循证实践建议与未来研究方向 本研究结果可综合 Ekelund 等 [117] 对久坐或体力活动与全因死亡率的关联分析,作为久坐的健康风险 参照标准(图 3-A) ,以基于风险状况选择不同的久坐间断策略(图 3-B) 。例如:中风险人群通过较高单 次负荷量的低~中强度运动以特定频率进行间断,低风险与部分中风险人群(青壮年等)可尝试考虑通过 高强度运动 [100,101] 或低量(<5 min)高强度间歇训练 [118] 间断久坐以累积运动量 [119] ,进而促进心脏代谢健 康 [17] 与体成分改善。图 3-C 总结了递增策略每一级的训练建议,不同人群还可依据不同糖、脂代谢与血 管功能促进目标参考本研究结果与讨论部分。 图 3 风险参考矩阵与久坐间断"台阶式"递增策略 ...
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目的:系统综述运动间断久坐对糖、脂代谢与血管功能的急性影响,并梳理其科学机理,提供循证应用建议。方法:检索Pubmed等四个数据库,使用Cochrane工具评估偏倚风险,审查纳入文献的方法学质量。由于纳入文献在受试者、结局指标与干预方案存在高度异质性,因此未使用荟萃分析定量合成证据。结果:共纳入59篇随机交叉试验文献,受试者共1214人。偏倚风险主要为实施与测量偏倚,部分研究在受试者纳入与方案设计上存在方法学问题。健康人群中,多数研究支持运动间断久坐能降低餐后血糖、胰岛素与血脂,并改善收缩压、舒张压、血流量与剪切应力。临床人群中,多数研究支持运动间断久坐有效降低餐后血糖、胰岛素,也能够降低收缩压、舒张压、平均动脉压、血流量与剪切应力,但难以改善血脂。涉及血流介导的血管舒张功能的研究极少且结果不一致,难以得出具体结论。结果差异主要源自受试者与干预方案差异。运动间断久坐相关科学机理可能与蛋白质转运、调节激素分泌和动作力学模式相关。结论:运动间断久坐能抵消久坐的不利影响,并急性改善糖、脂代谢与血管功能。未来应考虑更多元应用情景、人群与结局,探究间断的量-效关系并整合电子提醒等环境干预策略,方法设计需基于循证且亟待规范,确定核心测量指标及工具以降低测量结果异质性,检测更直接的生物标记物及其信号通路变化,通过效应-多组学-分子-功能等整合范式以识别心血管代谢潜在风险因素间的协同联系。
... Additionally, Little (2019) found that both ES and low-volume SIT could improve VO 2 peak and aerobic time trial performance. Meanwhile, engaging in ES multiple times during the day has demonstrated acute enhancements in glucose and lipid metabolism (Wolfe et al. 2020;Rafiei et al. 2021), and breaking up prolonged sitting with ES has been observed to counteract the adverse effects of sedentary on vascular function (Caldwell et al. 2021). Note that while the above studies were all supervised training and focused on efficacy, whereas relatively fewer investigations have been carried out in "real-world" environments, including workplaces (Wun et al. 2020) or using supervised stair climbing (Jenkins et al. 2019;Caldwell et al. 2021;Rafiei et al. 2021). ...
... Given that ES constitutes a minimal-volume exercise, comparing it with MICT may reveal its time-efficiency. Secondly, although ES has demonstrated acute enhancements in postprandial fat oxidation (Wolfe et al. 2020), there are no studies examining how this training approach impacts adaptations in fat metabolism. Given the strong link between fat oxidation rate and metabolic risk factors such as metabolic flexibility and insulin sensitivity (Goodpaster and Sparks 2017;Yang et al. 2022), it is critical to determine how ES impacts maximal fat oxidation (MFO), a concept that is the maximal value of whole body fat oxidation during exercise (Achten et al. 2002). ...
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The aims of this study were (1) to determine how stair-climbing-based exercise snacks (ES) compared to moderate-intensity continuous training (MICT) for improving cardiorespiratory fitness (CRF), and (2) to explore whether ES could improve maximal fat oxidation rate (MFO) in inactive adults. Healthy, young, inactive adults (n: 42, age: 21.6 ± 2.3 years, BMI: 22.5 ± 3.6 kg·m⁻², peak oxygen uptake (VO2peak): 33.6 ± 6.3 mL·kg⁻¹·min⁻¹) were randomly assigned to ES, MICT, or Control. ES (n = 14) and MICT (n = 13) groups performed three sessions per week over 6 weeks, while the control group (n = 15) maintained their habitual lifestyle. ES involved 3 × 30 s “all-out” stair-climbing (6 flight, 126 steps, and 18.9 m total height) bouts separated by >1 h rest, and MICT involved 40 min × 60%–70% HRmax stationary cycling. A significant group × time interaction was found for relative VO2peak (p < 0.05) with ES significantly increasing by 7% compared to baseline (MD = 2.5 mL·kg⁻¹·min⁻¹ (95% CI = 1.2, 3.7), Cohen’s d = 0.44), while MICT had no significant effects (MD = 1.0 mL·kg⁻¹·min⁻¹ (−1.1, 3.2), Cohen’s d = 0.17), and Control experienced a significant decrease (MD = −1.7 mL·kg⁻¹·min⁻¹ (−2.9, −0.4), Cohen’s d = 0.26). MFO was unchanged among the three groups (group × time interaction, p > 0.05 for all). Stair climbing-based ES are a time-efficient alternative to MICT for improving CRF among inactive adults, but the tested ES intervention appears to have limited potential to increase MFO.
... 。然而,传统运动由于其在环境、器材、时间和能力等方 面的特定要求,往往难以被大众人群接受或坚持 [4] 。例如:以高效著称的高强度间歇训练 (HIIT)能一定程度减少在器材与环境方面的参与障碍并节省时间,但其"高强度"与"不充 分间歇"的组合使得大部分久坐及代谢疾病人群难以坚持下去 [5] 。因此,如何在生活中以便 捷高效的方式获得与传统运动相似或更优的健康促进效果遂成为新的运动诉求。 碎片化运动(exercise snacks,ES,直译为运动零食)提供了一种新的思路。最新大规 模队列研究发现,每天碎片化的累积 3 次 1 min 剧烈强度活动,与显著降低 27%的全因死 亡风险 [6] 与 49%的心血管疾病风险相关 [7] 。其次,近 3 年的随机对照干预试验显示,每天 3 次孤立(次间隔≥1 h)的 20 s 骑行冲刺 [8][9] 或爬楼 [10] ,即可显著改善峰值摄氧量且比 HIIT 有 着更高的时间经济性,将 ES 应用于久坐间断也可抵消久坐对心血管代谢的负面影响 [11][12][13][14] ES 源自"累积运动",旨在将单次持续运动拆分为多次并孤立地分布于全天 [15] 。2007 年 之前的研究大多将 ES 设计为单次 10 min、全天累积的中强度运动 [16][17][18] 。随后,研究逐渐 缩短单次运动时长,并提升单次运动强度。Francois 等人于 2014 年首次在学术期刊中使用 "exercise snacks",用于描述在三餐前进行的低量 HIIT [19] 。这一系列研究发现,ES 与等量 持续运动有类似甚至更优的健康效益,且在日常生活中便于实施。鉴于此,世界卫生组织 也将"运动时间持续 10 min"的专家共识更新为"任何持续时间运动的健康效益都可被累积" [ Rafiei [11] , et al.2021 ...
... Wolfe [13] , et al.2020 ...
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碎片化运动(Exercise Snacks,ES)是以久坐间断和健康促进为目的,一天中多次孤立进行,强度中高至全力、单次持续时间≤1min或几个1min、次间间隔1-6h,对器材和环境要求低的一种运动策略。得益于ES“碎片化”和“生活化”的特征,其相较于传统运动具有更高的时间经济性、安排灵活性、运动愉悦感以及参与动机,并且安全。周期性应用ES可改善心肺适能、肌肉适能和体成分。作为久坐间断的干预措施,ES能抵消久坐对心血管代谢的不良影响并改善糖、脂代谢与血管功能。ES改善心肺适能可用中枢血流动力学适应与外周骨骼肌摄取及氧化重构进行解释,ES间断久坐改善糖、脂代谢与血管功能则与调节蛋白质转运、激素分泌与炎症等相关。兼具应用可行性和健康促进效果的双重优势使ES成为健康促进的新策略。未来研究应结合现代科技(如可穿戴设备),在办公室等真实环境中进行广泛调查与干预,并拓展更多类型人群与结局指标、探索其剂量效应及不同运动变量的影响及其作用机制。 Exercise snacks (ES) is an exercise strategy aimed at sedentary breaks and health promotion are performed in isolated bouts of moderate to all-out intensity exercises lasting ≤1 minute or several 1-minute sessions and performed periodically throughout the day with 1-6 hour intervals between sessions, and with low equipment and environmental requirements. The “snack” and “lifestyle” features of ES give it advantages in terms of time economy, flexibility of schedule, enjoyment of exercise, motivation to participate, and high adherence to exercise during the intervention, and it has also been shown to be safe. Long-term, regular ES improves cardiorespiratory fitness, muscle function, and body composition. As an intervention for sedentary breaks, ES counteracts the adverse effects of sedentary activity on cardiovascular metabolism and improves glucolipid metabolism and vascular function. ES improves cardiopulmonary fitness, as explained by central hemodynamic adaptation, peripheral skeletal muscle uptake, and oxidative remodeling. ES interruption of sedentary activity improves glucolipid metabolism and vascular function and is associated with the regulation of protein transport, hormone secretion, and inflammation. The combination of feasibility and health benefits makes ES a new strategy for health promotion. Future research should integrate modern technology to conduct a wide range of investigations and interventions in real-life situations such as schools, offices, and homes and to cover more types of people, explore dose effects and the impact of different exercise variables, expand outcome indicators, and explore the behavioral basis and physiological mechanisms.
... It is essential to avoid merging these distinct study designs, a practice that might potentially misguide readers. For example, recent meta-analyses indicate that sedentary breaks, based on cross-sectional designs, contribute to the reduction of blood glucose and insulin [23][24][25][26][27]. Furthermore, the available studies consistently demonstrate that high-intensity ES can improve blood lipids [2,3,7,17,28]. This amalgamation results in ambiguous conclusions regarding blood markers, primarily stemming from the inadequate delineation of various study designs, which may confound acute effects with long-term outcomes. ...
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We have suggested several lines of inquiry deserving of exploration for future research and discussion: I. It is imperative to establish an operational definition for ES [34]. Although this scoping review has conducted a preliminary exploration, we recommend conceptualizing ES as a variant of accumulated exercise and providing more specific criteria for intensity, duration, and inter-bout intervals. II. Defining and determining the intensity of ES poses a challenge. Traditional physiological variables are not optimized or validated to quantify such brief-duration exercise and subjective perceived fatigue or effort might serve as a pragmatic and feasible approach. Considering a variant of the “talk test” as an intensity measure for ES (requiring participants to be unable to speak normally during ES) is a perspective that warrants further investigation in future studies. III. The daily minimum or optimal dose for eliciting health benefits from ES remains undetermined. Establishing the minimum dose for eliciting health benefits would offer valuable practical information for individuals who subjectively perceive a "lack of time." IV. Current research has not rigorously controlled the inter-bout interval time for daily ES (which ranges from ~1-6 hours), making it challenging to propose a standardized reference value and understand whether different inter-bout intervals yield distinct health benefits. V. Existing studies have primarily focused on validating the efficacy of standalone ES. However, the potential synergies and enhanced benefits of combining ES with traditional structured exercises (such as resistance training) should not be overlooked. VI. Exploring the health benefits of ES in combination with specific physiological perturbations (e.g., blood flow restriction, hypoxia) is warranted, as these may present novel strategies for rehabilitation populations. VII. The long-term impact of ES on health benefits and physical activity remains unknown. Lastly, there is a need for further validation of the effectiveness of ES in "real-world" scenarios, such as schools, workplaces, and communities. In conclusion, we acknowledge the valuable work and contributions to this field by the authors. The purpose of writing this letter is to contribute to the discussion in this emerging research area, allowing for reflection that may lead to greater advances in future studies of this kind. We applaud the authors for conducting a scoping review on this topic, and encourage others to continue to study ES and other forms of intermittent physical activity for improving health.
... The concept of prolonged sitting is still relatively novel, but research is rapidly growing [7][8][9][10][11]13,17,18,[24][25][26][27][28]. The initial research on prolonged sitting predominantly includes the impact of interrupting prolonged sitting by various durations, intensities, and types of exercise on metabolic markers, the metabolic implications of chronic prolonged sitting, and prospective cohort studies [11,18,21,31,[55][56][57][58][59]. Still, a more detailed evaluation of the literature reveals several gaps and shortcomings. ...
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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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