J Appl Physiol 115: 1751–1756, 2013.
First published October 17, 2013; doi:10.1152/japplphysiol.00662.2013.
The effect of interrupting prolonged sitting time with short, hourly,
moderate-intensity cycling bouts on cardiometabolic risk factors in healthy,
young adults
Teatske M. Altenburg,1 Joost Rotteveel,2 David W. Dunstan,3,4 Jo Salmon,4 and Mai J. M. Chinapaw1
1
VU University Medical Center, EMGO Institute for Health and Care Research, Department of Public and Occupational
Health, Amsterdam, The Netherlands; 2VU University Medical Center, Department of Pediatrics, Pediatric Endocrinology,
Amsterdam, The Netherlands; 3Baker International Diabetes Institute Heart and Diabetes Institute, Physical Activity
Laboratory, Melbourne, Australia; and 4Deakin University, School of Exercise and Nutrition Sciences, Centre for Physical
Activity and Nutrition Research, Burwood, Australia
Submitted 10 June 2013; accepted in final form 11 October 2013
sedentary behavior; prolonged sitting; interrupted sitting; cardiometabolic risk
SEDENTARY BEHAVIOR [activities performed sitting during waking hours that typically require low-energy expenditure, i.e.,
1–1.5 times higher than rest (30)] has been identified as an
important and independent lifestyle risk factor for type 2
diabetes mellitus (T2DM) and cardiovascular disease (CVD) in
adults (14, 24, 25). A number of reviews have been published
about the association of sedentary behavior (e.g., television
Address for reprint requests and other correspondence: T. M. Altenburg, VU
Univ. Medical Center, EMGO Institute for Health and Care Research, Dept. of
Public and Occupational Health, van der Boechorststraat 7, 1081 BT, Amsterdam, The Netherlands (e-mail: [email protected]).
http://www.jappl.org
time, screen time, total sitting time) and cardiometabolic health
in adults (12, 28, 34).
Recent population-based studies suggest that prolonged,
unbroken sitting times, assessed by objective measures, such as
accelerometry, exert detrimental effects on cardiometabolic
biomarkers, irrespective of the total time spent sedentary and
total time spent in moderate- to vigorous-intensity physical
activity. For example, cross-sectional research has shown that
adults with a less-frequent number of interruptions in sedentary
time (prolonged sedentary time), on an average day, have a
poorer cardiometabolic risk profile, such as elevated waist
circumference, triglycerides, and 2-h plasma glucose, compared with those who had more frequent interruptions (breaks)
in their daily sedentary time (15).
A recent experimental study about the acute effects of
breaking up prolonged sitting in overweight/obese adults demonstrated that brief interruptions (i.e., 2-min walking interruptions every 20 min) to prolonged sitting significantly reduced
postprandial glucose and insulin levels compared with prolonged sitting (5). Importantly, these results were observed,
irrespective of the activity intensity (i.e., light or moderate
intensity) of the interruptions (5). Similarly, regularly (i.e.,
every 30 min) breaking up prolonged sitting with short (i.e.,
1-min, 40-s) bouts of physical activity significantly reduced
postprandial glucose and insulin levels in healthy, normalweight adults (26). These findings support the hypothesis that
the loss of contractile stimulation in weight-bearing muscles
may lead to a prolonged time in which cellular metabolism
substrates are present in the vascular compartments, underpinning the biological consequences of prolonged sitting (2, 13).
However, in contrast to the hypothesized mechanism, breaking
up prolonged sitting with regular, short bouts of physical
activity did not reduce postprandial triglycerides in healthy,
normal-weight adults (26).
To date, it is unclear whether less-frequent physical activity
interruptions (i.e., less than every 20/30 min) can exert similar
beneficial effects on cardiometabolic biomarkers, thereby approximating the recommendation of physical activity in short
sessions (1a). It is hypothesized that the loss of contractile
stimulation in weight-bearing muscles may underpin the detrimental consequences of prolonged sitting (2, 13). Therefore,
we aimed to examine whether hourly physical-activity interruptions in sitting time would attenuate possible detrimental,
acute effects on postprandial cardiometabolic biomarkers compared with prolonged, uninterrupted time spent sitting. Since
8750-7587/13 Copyright © 2013 the American Physiological Society
1751
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Altenburg TM, Rotteveel J, Dunstan DW, Salmon J, Chinapaw
MJ. The effect of interrupting prolonged sitting time with short, hourly,
moderate-intensity cycling bouts on cardiometabolic risk factors in
healthy, young adults. J Appl Physiol 115: 1751–1756, 2013. First
published October 17, 2013; doi:10.1152/japplphysiol.00662.2013.—Although detrimental associations of sitting time and health indicators
have been observed in young adults, evidence of pathophysiological
mechanisms is lacking. Therefore, this study tested the hypothesis that
the acute cardiometabolic effects of prolonged sitting can be compensated by hourly interruptions to sitting in healthy, young adults.
Additionally, leg muscle activation during sitting and moderateintensity physical activity interruptions was assessed. Eleven apparently healthy adults (18 –24 yr; five men/six women) participated in
this randomized, crossover study, involving two experimental conditions: 1) 8 h prolonged sitting and 2) 8 h of sitting, interrupted with
hourly, 8-min, moderate-intensity cycling exercise bouts. In both
conditions, participants consumed two standardized, high-fat mixed
meals after 1 and 5 h. Capillary blood samples were collected hourly
during each 8-h experimental condition. Muscle activity was measured using electromyography. Muscle activity during cycling was
seven to eight times higher compared with rest. Postprandial levels of
C-peptide were significantly lower (unstandardized regression coefficient ⫽ ⫺0.19; confidence interval ⫽ [⫺0.35; ⫺0.03]; P ⫽ 0.017)
during interrupted sitting compared with prolonged sitting. Postprandial levels of other cardiometabolic biomarkers (e.g., glucose, triglycerides, cholesterol) were not significantly different between conditions. Hourly physical activity interruptions in sitting time, requiring
a muscle activity of seven to eight times the resting value, led to an
attenuation of postprandial C-peptide levels but not for other cardiometabolic biomarkers compared with prolonged sitting in healthy,
young adults. Whether this acute effect transfers to chronic effects
over time is unknown.
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Cardiometabolic Effects of Prolonged Sitting
postprandial lipid responses to moderate- to vigorous-intensity
(continuous and intermittent) exercise bouts are demonstrated
to occur 13–18 h after completion of the exercise bout (9, 16,
20, 21, 26), changes in postprandial lipids, induced by interrupting prolonged sitting, might not be expected within 1 day.
Therefore, postprandial indicators of glucose metabolism were
defined as primary outcome measures, whereas postprandial
indicators of lipid metabolism were defined as secondary
outcomes. We assessed the amount of leg-muscle activation
corresponding to sitting and moderate-intensity physical-activity interruptions compared with resting muscle activity.
METHODS
Participants
Study Design
This crossover study included two acute experimental conditions of
8 h duration in a laboratory setting, was approved by the Medical
Ethics Committee of the VU University Medical Center in Amsterdam, and was in accordance with the Declaration of Helsinki. The
experimental conditions were: 1) prolonged sitting (SIT) and 2) sitting
with hourly interruptions of 8-min moderate-intensity cycling bouts
(SIT-CYCLE). To eliminate potential carryover effects, there was a
minimum washout of 7 days between each condition. The order of the
experimental conditions was assigned randomly.
Procedures
Experimental day protocol. After an 8-h fast, participants visited
the research room. During the first visit, the informed-consent document and a health history were completed, and baseline measurements
[blood measurements, anthropometrics, and muscle activity (details
below)] were collected [time (t) ⫽ 0]. The participants then sat quietly
for 1 h to achieve a “steady state.” Subsequently, participants consumed a standardized, high-fat mixed meal (for details, see Standardized meals below), which they were requested to drink within 10 min.
After consuming the standardized meal, in the SIT condition, participants remained seated in a comfortable, reclining lounge chair for the
next 7 h. They were allowed to use the computer with a DVD player
and internet access and reading materials. During the sitting, participants were instructed to minimize excessive movement but were
allowed to visit the toilet. In the SIT-CYCLE condition, 1 h after the
initial 1-h steady-state period and the standardized meal, participants
completed an 8-min moderate-intensity cycling bout every hour,
approximating the recommendation of physical activity in short sessions (1a). This procedure was repeated five times, resulting in a total
cycling duration of 48 min. All participants consumed a second
standardized, high-fat mixed meal after 5 h of sitting (t ⫽ 5). For the
SIT-CYCLE condition, the cycling bout was performed directly after
the meal was consumed. Blood samples were collected hourly during
each 8-h experimental condition (i.e., nine blood samples). In the
Altenburg TM et al.
SIT-CYCLE condition, blood samples were taken just before the
onset of the cycling bouts to eliminate the acute effects of the
moderate-intensity cycling bout.
Cycling bouts. The cycling bouts were undertaken on a programmable cycle ergometer in the research room under the supervision of
the research staff. Moderate-intensity cycling intensity was determined using the Karvonen formula (17). According to this formula,
target heart rate (HR) was determined via the HR reserve (HRR) by
using the formula: target HR ⫽ {[% HRR/(maximum HR ⫺ resting
HR)] ⫹ resting HR}. In this formula, maximum HR was assumed to
be equal to 220 minus age (year). Resting HR was obtained after the
participant had rested for 10 min in a lying position (during baseline
measurements). Moderate intensity was defined as 40 – 60% HRR (1).
HR was monitored continuously during the cycling bouts (Polar
RS100; Polar Electro Oy, Kempele, Finland). Perceived exertion at
the end of each cycling bout was monitored further using the Borg rate
of perceived exertion (RPE) scale.
Standardized meals. Participants were studied in a postprandial
state, as this was considered to be more representative of “normal
daily life” than the fasted state. The importance of studying the
postprandial state is emphasized further by evidence that the peaks in
glucose and lipids induced by high-calorie meals are associated with
biochemical inflammation, endothelial dysfunction, and sympathetic
hyperactivity (3, 4, 7, 22). Moreover, when repeated multiple times
each day, these peaks in glucose and lipids increase the risk for
atherosclerosis and CVD (22). Participants consumed two standardized meals during the experimental sitting days. The first standardized, high-fat mixed meal (i.e., breakfast), given after the 1st h of
steady-state sitting, consisted of approximately 58.8 g fat, 92.0 g
carbohydrates, and 15.6 g proteins (in total, 843 kcal). The second
standardized, high-fat mixed meal (i.e., lunch), given after 5 h of
sitting, consisted of approximately 77.1 g fat, 116.7 g carbohydrates,
and 27.7 g proteins (in total, 1,190 kcal). The fat, carbohydrate, and
protein content of the standardized meals was based on a previous
study of our group in young adults, demonstrating postprandial
increases in levels of HDL cholesterol, triglyceride, insulin, and
glucose (29).
Measurements
Anthropometry. Body height, body weight, and waist circumference were measured according to a standardized protocol. Body
height was measured with a Seca Leicester portable stadiometer with
an accuracy of 0.1 cm. Body weight was measured with a calibrated
electronic scale (Seca 861), with an accuracy of 0.1 kg. Waist
circumference was measured with a flexible band (Seca 200) at the
level of the umbilicus, with an accuracy of 0.5 cm.
Blood measurements. Capillary blood was collected using a validated collection kit developed for ambulatory purposes (Demecal
Europe, Haarlem, The Netherlands). In short, after a finger prick, ⬃60
␮l capillary blood is absorbed by a sponge and transferred to a
collection tube containing 220 ␮l dilution buffer. After mixing, the
diluted blood is filtered, producing approximately eight times diluted
isolated plasma. Capillary samples were sent to the laboratory by
regular mail, stored at 4°C within 24 h, and analyzed within 48 h. All
cardiometabolic biomarkers were measured using an ADVIA 1650
analyzer and accompanying reagents (Siemens Healthcare Diagnostics, Tarrytown, NY), except for the free glycerol triglyceride assay
(Mizuho Medy, Tosu City, Saga, Japan). Although this Demecal
capillary blood-sampling method had reduced accuracy, previous
research showed that it can be considered as a valid alternative for
venous blood sampling, with good stability during transportation (10).
Cardiometabolic biomarkers included plasma triglycerides, glucose,
total cholesterol, HDL cholesterol, LDL cholesterol, and C-peptide
and were determined in all capillary samples. Unfortunately, for two
participants, data for one blood sample were missing.
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Five men and six women, aged 18 –24 yr, participated in this study.
Participants were recruited through distribution of flyers, announcements on university websites, and Dutch recruitment websites. Participants were included if they were of normal weight and apparently
healthy, were Dutch or English speaking, and signed an informed
consent. Exclusion criteria were major illness/injury and physical
problems that may limit the ability to perform the experiment. Participants were screened by a health-check questionnaire, including
questions about participants’ medical history (e.g., heart/kidney/joint/
muscle/asthmatic complaints, coagulation problems, chest pain).
Moreover, they were requested to refrain from any moderate- to
vigorous-intensity physical activity for at least 72 h before the experiment and to avoid drinking alcohol and smoking for at least 24 h
before the experiment.
•
Cardiometabolic Effects of Prolonged Sitting
Statistics
Descriptive participant characteristics [median (minimum/maximum)] were calculated at baseline. Data were not distributed normally, and Wilcoxon signed-rank tests were used to test for differences between conditions at baseline and also to test for differences
between EMG during sitting and rest and during rest and cycling. The
average of the blood samples at t ⫽ 0 and at t ⫽ 1 (i.e., at the
beginning and the end of the 1st h) was considered as steady state and
used as baseline blood sample.
Generalized estimating equations (GEE) were used to assess the
difference between prolonged and interrupted sedentary time for each
cardiometabolic biomarker. All assumptions of the GEE models were
met, indicating that GEE analysis was appropriate for the data of the
current study. This longitudinal analysis technique was used to correct
for dependency within the repeated measures (i.e., eight blood samples and two conditions) for each participant. Since we used a
crossover design in this study, we did not adjust for demographic
variables, such as age, gender, and weight status. All statistic procedures were performed using SPSS software (version 18.0). Statistical
significance was set at P ⬍ 0.05.
RESULTS
Table 1 shows the baseline participant characteristics. Baseline steady-state blood values for triglycerides, glucose, total
cholesterol, HDL cholesterol, LDL cholesterol, and C-peptide
were not different between the SIT and SIT-CYCLE conditions. The intensity of the cycling bouts in the SIT-CYCLE
condition was, on average, 52.0 ⫾ 3.2% HRR, indicating that
the physical activity interruptions were performed at the intended, moderate intensity. Borg RPE scores were, on average,
11.2 (SD 1.6), ranging from seven to 15.
Figure 1 demonstrates levels of all cardiometabolic biomarkers throughout 1 day of prolonged sitting and 1 day of inter-
1753
Altenburg TM et al.
Table 1. Descriptive participant characteristics [median
(25th–75th percentile); n ⫽11]
Baseline Anthropometrics
Age, years
Gender, % men
Height, cm
Weight, kg
BMI, kg/m2
Waist circumference, cm
Triglycerides, mmol/l
Total cholesterol, mmol/l
HDL cholesterol, mmol/l
LDL cholesterol, mmol/l
Glucose, mmol/l
C-peptide, mmol/l
21.4 (19.5–23.1)
45
175.8 (169.5–184.8)
71.8 (65.4–75.0)
23.2 (20.1–26.1)
79.7 (71.7–82.9)
Steady-State SIT
Steady state SIT-CYCLE
0.60 (0.55–0.90)
3.75 (3.40–4.00)
1.10 (0.95–1.40)
1.90 (1.55–2.05)
4.25 (4.05–4.70)
0.57 (0.48–0.66)
0.90 (0.65–1.1)
3.75 (2.95–3.90)
1.10 (0.95–1.20)
1.95 (1.50–2.20)
4.50 (4.30–4.85)
0.62 (0.57–0.76)
Baseline, 1st visit; BMI, body mass index; SIT, sitting only condition;
SIT-CYCLE, sitting and hourly physical activity interruptions; steady state,
value after 1st h of sitting [e.g., time (t) ⫽ 0 and t ⫽ 1]. Baseline steady-state
blood values were not significantly different between the SIT and SIT-CYCLE
conditions.
rupted sitting. GEE analysis for the 7-h period (e.g., including
the response to both standardized meals) revealed that C-peptide levels were significantly higher during prolonged vs.
interrupted sitting (unstandardized regression coefficient ⫽
⫺0.19; confidence interval ⫽ [⫺0.35; ⫺0.03]; P ⫽ 0.017;
Table 2). Levels of triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol, and glucose were not different between the SIT and the SIT-CYCLE conditions (Table 2). GEE
analysis for the 4-h response (e.g., including the response to the
first standardized meal only) revealed similar results.
Average rectified EMG of the RF and GAS muscles during
sitting was not significantly different from resting EMG (Table 3).
During the moderate-intensity cycling interruptions, averaged
rectified EMG was seven times the resting EMG for the RF
muscle (P ⬍ 0.05) and eight times the resting EMG for the
GAS muscle (P ⬍ 0.05).
DISCUSSION
Relative to prolonged sitting, brief, hourly moderate-intensity, 8-min physical activity interruptions in sitting time were
associated with significantly lower postprandial plasma levels
of C-peptide but not of other cardiometabolic biomarkers in
healthy young adults. EMG, during the moderate-intensity
physical activity interruptions, was seven to eight times the
resting values.
The lower levels of postprandial C-peptide, reflecting reduced endogenous insulin secretion (27, 37), during interrupted
sitting compared with prolonged sitting, are comparable with
previous findings in overweight and obese adults (5) and in
healthy, normal-weight adults (26). Dunstan et al. (5) found
that interrupted (i.e., 2-min bouts of walking every 20 min)
sitting time reduces postprandial insulin levels by 23% in
overweight/obese adults. Similarly, Peddie et al. (26) demonstrated that breaking up prolonged sitting (i.e., 1-min, 40-s
bouts of walking every 30 min) reduced postprandial insulin
levels by 26% in healthy, normal-weight adults. The present
study shows that interrupting prolonged sitting every hour may
also be important for acute health outcomes in young and
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Muscle activity. Since it is hypothesized that the loss of contractile
stimulation in weight-bearing muscles underlies the consequences of
prolonged sitting (2, 13), we measured muscle activity of the rectus
femoris (RF), vastus lateralis, and gastrocnemius (GAS) muscles
using electromyography (EMG). Previous studies have shown that
EMG amplitude is a reliable measure of muscle activation (32, 35),
both during short- and long-term intervals (18). After shaving and
cleaning the skin with 70% ethanol, two electrodes (lead-off area 1.0
cm2; Blue Sensor; Ambu, Ølstykke, Denmark) were placed on the
belly of each muscle in a bipolar configuration (interelectrode distance
of 25 mm). A reference electrode was placed on the patella.
At the beginning of each experimental condition (during baseline
measurements), participants were asked to lie down for 10 min to
obtain resting EMG values. EMG recordings of 30 min were made
three times during sitting (both conditions; after 1, 3, and 5 h of
sitting), and 8-min EMG recordings were made during all cycling
bouts (SIT-CYCLE condition). EMG signals were amplified (⫻1,000)
with a biosignal amplifier (0.01–10 kHz; input impedance 110 M⍀;
g.tec), analog-to-digital converted with a Simultaneous Sampling
AtoD board (PCI-6143; National Instruments, Austin, TX), digitized
(10 kHz), band-pass filtered (10 – 400 Hz), and stored with the torque
signal on a computer disk. Rectified EMG signals during the sitting
periods and the cycling bouts were averaged over a time period of 20
and 6 min, respectively (e.g., time interval in which rectified EMG
was stable), and expressed as percentage of the resting rectified EMG.
However, due to noise caused by movement of the EMG wires, we did
not attain reliable EMG data for all participants and during all
measures. Therefore, participant numbers varied between conditions
and muscles, and signals were sometimes averaged over a shorter time
period (range: 5–20 min during sitting periods and 2– 6 min during
cycling bouts).
•
Cardiometabolic Effects of Prolonged Sitting
B
4.0
3.0
2.0
1.0
0.0
0
1
2
3
6
7
8
D
LDL cholesterol,
mmol/l
HDL cholesterol,
mmol/l
5
2.00
1.50
1.00
0.50
0
E
4
Time, hr
C
1
2
3
4
5
Time, hr
6
7
8
6.5
5.5
4.5
3.5
0
1
2
3
4
5
6
7
8
4.0
3.5
3.0
2.5
0
1
Table 2. Difference (B and 95% CI) in cardiometabolic
biomarkers between prolonged and interrupted sedentary
time
B [95% CI]
Triglycerides, mmol/l
Total cholesterol, mmol/l
HDL cholesterol, mmol/l
LDL cholesterol, mmol/l
Glucose, mmol/l
C-peptide, mmol/l
0.19 [⫺0.18; 0.57]
⫺0.05 [⫺0.28; 0.18]
⫺0.04 [⫺0.11; 0.03]
0.11 [⫺0.14; 0.16]
⫺0.03 [⫺0.17; 0.11]
⫺0.19 [⫺0.35; ⫺0.03]*
B, unstandardized regression coefficient; CI, confidence interval. Note that
a negative B indicates a lower blood level for the SIT-CYCLE condition
compared with the SIT condition. *Significant difference between conditions
(P ⬍ 0.02).
3
4
5
6
7
8
6
7
8
Time, hr
2.5
2.0
1.5
1.0
0
1
2
3
4
5
4.0
*
3.0
2.0
1.0
0.0
0
Time, hr
healthy adults. Although the effect of 1 day of prolonged
sitting on levels of C-peptide may seem small, it may have
considerable health risks when accumulated for multiple days.
In contrast to the findings from Dunstan et al. (5) and Peddie et
al. (26), we did not observe a lowering of postprandial glucose
during interrupted sitting compared with prolonged sitting.
This might be related to the capillary blood-sampling method,
which has been shown to differ (range: 0.1– 0.3 mmol/l for
fasting glucose) from venous blood sampling for glucose
measurements (10, 19). Another possible explanation for the
contrasting findings could be the different study samples. Our
sample consisted of healthy, young adults, whereas overweight
and obese, older adults (45– 65 yr old) participated in the study
of Dunstan et al. (5). The higher insulin sensitivity in our
young participants makes it more difficult to detect conditionrelated changes in insulin sensitivity. However, participants in
the study of Peddie et al. (26) were, although slightly older (4.5
yr), comparable with our participants.
2
Time, hr
F
7.5
4.5
1
2
3
4
5
6
7
8
Time, hr
In line with the findings of Peddie et al. (26), we did not
observe any differences in postprandial triglycerides during
sitting with hourly physical-activity interruptions compared
with prolonged sitting. In addition, we did not observe any
differences in postprandial total cholesterol, HDL cholesterol,
and LDL cholesterol during interrupted sitting compared with
prolonged sitting. These findings are in contrast with one of the
hypothesized mechanisms underlying the biological consequences of prolonged sitting, suggesting that loss of local
contractile stimulation in weight-bearing muscles leads to the
suppression of skeletal muscle lipoprotein lipase (LPL) activity
(2, 13). The acute loss of LPL activity at the vascular endothelium impairs several aspects of lipid metabolism (23) and
may contribute to cardiometabolic risk over sustained periods
of time (i.e., years or indeed, a lifetime). In our study population, the standardized, high-fat mixed meals induced only
slight increases in triglycerides, total cholesterol, HDL cholesterol, and LDL cholesterol, possibly reflecting the relatively
“metabolically healthy” profile of our participants. This may be
Table 3. Rectified EMG as percentage of resting EMG
during prolonged sitting (SIT) and during sitting with hourly
physical activity interruptions (SIT-CYCLE; n ⫽ 8)
Muscle
Condition
Rectus femoris muscle
EMG during Sitting EMG during Cycling
SIT
SIT-CYCLE
1.74 ⫾ 2.02
0.90 ⫾ 0.27
NA
7.14 ⫾ 2.96*†
SIT
SIT-CYCLE
1.54 ⫾ 1.68
1.49 ⫾ 0.77
NA
8.14 ⫾ 4.50*‡
Gastrocnemius muscle
EMG, electromyography. *Significantly different from 1.0 (i.e., mean resting EMG value); †n ⫽7; ‡n ⫽ 6.
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Glucose, mmol/l
Fig. 1. Levels of cardiometabolic biomarkers
(A–F) throughout 1 day of prolonged sitting
(closed circles; SIT) and 1 day of interrupted
sitting (open circles; SIT-CYCLE). Note
that baseline measurements were not significantly different between time points [time
(t) ⫽ 0 and t ⫽ 1] and experimental days
(SIT and SIT-CYCLE). Standardized, highfat meals were consumed at t ⫽ 1 and t ⫽ 5.
*Significant higher levels of C-peptide for
SIT-CYCLE compared with SIT condition
(P ⬍ 0.05).
Altenburg TM et al.
Total cholesterol,
mmol/l
Triglycerides,
mmol/l
A
•
C-peptide, mmol/l
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Cardiometabolic Effects of Prolonged Sitting
Altenburg TM et al.
1755
A limitation of our study was the capillary blood-sampling
method, which is considered to be inferior to venous blood
sampling, although this method is considered to be a valid
alternative to venous blood sampling, as linear regression
analysis revealed that slopes differed no more than 10% from
1.0 (representing near-perfect agreement), except for glucose
(10). This should be kept in mind when interpreting our results.
Another limitation is the small sample size, which could
explain the lack of statistical significance for postprandial
glucose and blood lipids. Finally, we were unable to obtain
information on the level of hydration during the physicalactivity interruptions, which might have influenced the measurement precision of the assessed cardiometabolic biomarkers.
We conclude that short, hourly, moderate-intensity physical-activity interruptions to prolonged sitting, requiring
muscle activity of the weight-bearing muscles of seven to
eight times the resting value, may prevent increases in
postprandial levels of C-peptide. It is important that detrimental cardiometabolic effects may already occur within 1
day of prolonged sitting, even in young and healthy adults.
Our findings further support recent suggestions for interrupting sitting time, in addition to meeting the physical
activity guidelines to prevent cardiometabolic risk (8). Future studies should examine different frequencies and durations of physical activity interruptions to prolonged sitting
and effects on cardiometabolic health to determine the most
advantageous pattern of prolonged vs. interrupted sitting in
preventing cardiometabolic risk.
GRANTS
Support for D. W. Dunstan is provided by a Future Fellowship from the
Australian Research Council. Support for J. Salmon is provided by a Principal
Research Fellowship from the National Health and Medical Research Council
(IDAPP1026216).
DISCLOSURES
The authors declare no conflicts of interest.
AUTHOR CONTRIBUTIONS
Author contributions: T.M.A., D.W.D., J.S., and M.J.M.C. conception and
design of research; T.M.A. performed experiments; T.M.A. analyzed data;
T.M.A., J.R., D.W.D., J.S., and M.J.M.C. interpreted results of experiments;
T.M.A. prepared figures; T.M.A. drafted manuscript; T.M.A., J.R., D.W.D.,
J.S., and M.J.M.C. edited and revised manuscript; T.M.A., J.R., D.W.D., J.S.,
and M.J.M.C. approved final version of manuscript.
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one explanation for the lack of significant effects of prolonged
vs. interrupted sitting on these parameters. A second possible
explanation might be that longer uninterrupted sitting time than
what was used (⬎8 h) may be needed to detect significant
detrimental changes in this measure. Previous studies about the
effects of exercise bouts on postprandial triglycerides demonstrated that postprandial lipid responses generally occur ⬎13 h
after completing moderate- to vigorous-intensity (continuous
or intermittent) exercise (9, 16, 20, 21, 26). Additionally,
skeletal muscle LPL activity is thought to peak ⬎8 h after
exercise (31).
Stephens et al. (33) tested the hypothesis that the negative
health effects of sitting may be partly due to a positive energy
balance. They demonstrated that 1 day of sitting considerably
reduced insulin action relative to continuous standing/light
ambulation; however, this effect was minimized but not prevented when energy intake was reduced to match expenditure.
Additionally, when controlling for sitting time, physical exercise, and daily energy expenditure, Duvivier et al. (6) demonstrated that the adverse effects of sitting on insulin sensitivity
and plasma lipids could not be compensated by 1 h of daily
continuous physical activity. Due to these distinctive differences in study design and specific research questions, the
results of our study cannot be compared with the studies
mentioned above. Additionally, another major distinction is
that the participants in our study were assessed while in a
postprandial state (i.e., throughout 1 day of prolonged and 1
day of interrupted sitting), whereas the participants in the
studies of Stephens et al. (33) and Duvivier et al. (6) were
assessed in a fasted state (i.e., the morning after the experimental conditions).
Activity of the RF muscle during sitting varied considerably,
although not significantly, between the 2 experimental days
(e.g., 1.7 and 0.9 times the resting values). An explanation
could be that the electrode placement for the RF muscle was
slightly different between the experimental days, which may
have affected the EMG measurement (11, 18). Furthermore, all
participants performed the physical activity bouts within the
targeted range of 40 – 60% HRR, i.e., moderate intensity, with
HRR varying between 46% and 57% HRR.
A strength of our study and novel aspect included the
measurement of muscle activity of the GAS and RF weightbearing muscles in young adults. Since the biological mechanism underlying the health consequences of prolonged sitting
suggests the necessity of muscle activity, it is important to
establish how much muscle activity is sufficient to attenuate
these consequences. As the present study only collected these
data from a subsample of participants, it was not possible to
examine whether muscle activity potentially mediated the
effects of interrupted sitting on health outcomes. This could be
examined in future research. Another strength was the focus on
the effects of prolonged vs. interrupted sitting on lipid metabolism, which have not been reported to date. Our sample of
healthy, young (18 –24 yr) adults is an additional strength of
our study, since it is less likely to be influenced by confounding
effects, such as aging and disease progression (e.g., obesity,
T2DM). The crossover design also strengthens our study. By
experimentally imposing 8 h of sitting and 8 h of interrupted
sitting in a separate session (assigned randomly), we were able
to study the effects of prolonged vs. interrupted sitting in a
systematic way.
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9.
Cardiometabolic Effects of Prolonged Sitting