Eur J Appl Physiol (2016) 116:77–84

DOI 10.1007/s00421-015-3224-7

ORIGINAL ARTICLE

The training and detraining effect of high‑intensity interval

training on post‑exercise hypotension in young overweight/obese
women
Biggie Bonsu1 · Elmarie Terblanche1

Received: 16 February 2015 / Accepted: 16 July 2015 / Published online: 21 August 2015
© Springer-Verlag Berlin Heidelberg 2015

Abstract clinically significant following post- and detraining (4.26

Purpose Studies evaluating the response in blood pres- and 3.87 mmHg, respectively).
sure (BP) following high-intensity interval training (HIIT) Conclusion The findings suggest that six HIIT sessions
are scant even though there has been extensive work done is sufficient to affect clinically significant PEH responses
on the BP response following acute and chronic low- to in young, overweight/obese women; however, the training
moderate-intensity aerobic and resistance exercise in both effects are lost within 2 weeks of detraining.
hypertensive and normotensive individuals. The present
study sought to investigate the training and detraining Keywords Blood pressure · High-intensity interval
effects of short-term HIIT on the post-exercise hypotension training · Detraining
(PEH) response in overweight/obese young women.
Method Twenty young untrained women volunteered for Abbreviations
the study. Participants performed six HIIT sessions on a ANOVA Analysis of variance
treadmill within 2 weeks (week 1: 10 × 1 min and week b.min−1 Beats per minute
2: 15 × 1 min intervals at 90–95 % HRmax, separated by BMI Body mass index
1 min active recovery at 70 % HRmax each session) and BP Blood pressure
detrained for 2 weeks. Post-exercise BP was measured for cm Centimeter
1 h following the first and last HIIT sessions. DBP Diastolic blood pressure
Results Participants were normotensive (SBP: ES Effect size
119.2 ± 5.60 mmHg; DBP: 78.8 ± 4.12 mmHg) and had a HIIT High-intensity interval training
BMI greater than 25 kg m−2. The magnitude of the systolic HR Heart rate
hypotensive response was slightly greater after the six ses- HRmax Maximum heart rate
sions HIIT compared to pre-training (5.04 and 4.28 mmHg, i.e. That is
respectively), and both would be considered clinically sig- kg Kilogram
nificant (>3 mmHg decrease). After 2 weeks, detraining the Kg m−2 Kilogram per square meter
PEH response was not clinically significant (1.08 mmHg min Minute
decrease). The magnitude of the DBP response was only ml kg−1 min−1 Milliliters per kilogram body weight per
minute
Communicated by Massimo Pagani. mmHg Millimeters mercury
PAR-Q Physical activity readiness questioner
* Biggie Bonsu PEH Post-exercise hypotension
bbonsu.chs@knust.edu.gh
SBP Systolic blood pressure
Elmarie Terblanche SD Standard deviation
et2@sun.ac.za
Sec Second
1
Department of Sport Science, Stellenbosch University, TPR Total peripheral resistance
Matieland, Private Bag X1, Stellenbosch 7602, South Africa VO2max Maximal aerobic capacity

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78
Introduction
The worldwide increase in rates of urbanization is associ-
ated with modifications in human behavior and has led to
a high prevalence of sedentary lifestyles (Cornelissen et al.
2010). Despite the known health benefits of exercise (Mor-
row et al. 2004), it remains a challenge for most people to
engage in regular physical activity. Among other cardio-
vascular risk factors, obesity is an independent risk factor
for the development of hypertension (Hamer and Boutcher
2006; Kopelman 2000). Evidence shows that the arterial
pressure response to exercise is aggravated in obese com-
pared with lean adults (Dipla et al. 2012). Likewise, inac-
tive persons have a 30–50 % higher risk for developing
hypertension (American Heart Association 1999; Whelton
et al. 2002).
Various forms of physical activity has been shown to
reduce BP in both hypertensive and normotensive indi-
viduals (Brandão Rondon et al. 2002; Eicher et al. 2010;
Keese et al. 2012; Millen et al. 2013; Simão et al. 2005;
Tjønna et al. 2009; Whyte et al. 2010). This phenomenon
which is generally known as post-exercise hypotension,
defined as the reduction in BP below resting levels during
recovery from exercise (Kenney and Seals 1993; Rossow
et al. 2010), has been widely investigated during low- to
moderate-intensity endurance and resistance exercise train-
ing protocols (Bennett et al. 1984; Brownley et al. 1996;
Cléroux et al. 1992; Cornelissen et al. 2010; Floras et al.
1989; Floras and Wesche 1992; Forjaz et al. 2000, 2004;
Guidry et al. 2006; Hagberg et al. 1987; Hara and Floras
1994; Hua et al. 2009; Pescatello et al. 1991, 1999, 2007;
Piepoli et al. 1994; Quinn 2000; Teixeira et al. 2011). In
general, researchers are in agreement that both acute and
chronic exercise training lead to clinically significant PEH
responses in adults and that the blood pressure lowering
effects of exercise are more pronounced in those with the
highest initial blood pressure (Brandão Rondon et al. 2002;
Cardoso et al. 2010; Pescatello and Kulikowich 2001). A
popular training method that has not yet been associated
with a PEH response is high-intensity interval training.
Kemi and Wisløff (2010) describes high-intensity inter-
val training (HIIT) as an exercise training method that is
characterized by short (10 s to 5 min), repeated bouts of
vigorous activity, executed at or near peak oxygen uptake,
and interspersed by periods of rest or low-intensity exer-
cise. The idea behind HIIT is to allow the physiological
systems to be overloaded with exercise intensities greater
than those achieved during a progressive maximal aerobic
capacity test (Stuckey et al. 2011) by separating the work
done in rest intervals (Kemi and Wisløff 2010). HIIT has
been described as a time-efficient training strategy which
could serve as motivation for individuals who claim lack
of time as the major reason for not adhering to a training
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Eur J Appl Physiol (2016) 116:77–84
regime. Even though some studies have shown the meta-
bolic and cardiovascular benefits of HIIT (Burgomaster
et al. 2008; Rakobowchuk et al. 2008), there have been
limited studies on the training effects of HIIT on the BP
response following exercise (Liu et al. 2012; Rossow et al.
2010). Therefore, the purpose of this study was to investi-
gate the training and detraining effects of short-term HIIT
on the post-exercise hypotension response in overweight/
obese young women.
Methods
Twenty young (21.2 ± 1.9 years) and overweight/obese
(BMI: 29.0 ± 3.1 kg m−2) women volunteered to partake
in this study. Participants were considered healthy and
normotensive (119.2 ± 5.6/78.8 ± 4.12 mmHg), and they
were considered sedentary (exercised less than 1 day per
week). Signed informed consent was obtained from all
individuals prior to any testing or measurements. Partici-
pants also completed a physical activity readiness question-
naire (PAR-Q) to ensure that training would not aggravate
any health condition. The study was approved by the Ethics
Committee of Research Subcommittee A at Stellenbosch
University, South Africa.
A calibrated electronic scale (UWE BW-150, Bris-
bane, Australia) was used to measure body mass which
was recorded to the nearest 0.1 kg, while height was taken
using a standing stadiometer (Seca, Germany). Height
was recorded in centimeters to one decimal place (0.1 cm)
according to the International Standards for Anthropomet-
ric Assessment (Marfell-Jones et al. 2006). The body mass
index (BMI = kg m−2) was calculated from height and
body mass. Body composition was measured by bioelectri-
cal impedance analysis with a Quadscan 400 Bodystat unit
(Isle of Man United Kingdom). Resting BP and heart rate
(HR) were taken with an ambulatory BP monitor (Ergoline
Ergoscan 2008, Germany) after a 5-min seated rest period.
The average of three BP readings was taken provided that
these readings differed by no more than 5 mmHg.
Individuals performed an incremental exercise test to
exhaustion on the h/p/cosmos Saturn treadmill (Nussdorf-
Traunstein, Germany) to determine their maximal aerobic
capacity (VO2max). A COSMED® Quark CPET (Rome,
Italy) metabolic system was used to continuously monitor
gas exchange variables. The COSMED® CPET heart rate
monitor was also used to monitor HR. Individuals’ safety
on the treadmill was secured by an adjustable body safety
harness. The test was ended if there were any visible test
termination criteria as defined in the ACSM’s guidelines for
exercise testing and prescription (ACSM 2010) or upon the
individual’s demand to stop the test. The outcome of each
participant’s VO2max test was used to determine the running
Eur J Appl Physiol (2016) 116:77–84 79

velocity equivalent to 90–95 % of HRmax for the HIIT exer- Table 1  Physical and physiological characteristics of the participants
cise sessions. Blood pressure and heart rate were meas- Variables Mean ± SD Range
ured 10 min following the VO2max test and continuously
at 10 min intervals over an hour recovery period, using the Age [years] 21.2 ± 1.93 19.0–25.0
ambulatory blood pressure monitor (Ergoline, Ergoscan Height [cm] 160.0 ± 6.70 145.8–172.7
2008, Germany). Weight [kg] 74.3 ± 10.0 61.0–103.1
The training intervention comprised six sessions of BMI [kg.m−2] 29.0 ± 3.10 25.1–37.3
1-min running on the treadmill, interspersed by a minute Body fat [%] 35.5 ± 5.00 25.9–45.5
active recovery. The training session commenced with a Resting SBP [mmHg] 119.2 ± 5.60 108.0–129.0
5-min warm-up at a running velocity equivalent to 50 % Resting DBP [mmHg] 78.8 ± 4.12 71.0–89.0
HRmax, followed by 10 × 1-min bouts at 90–95 % HRmax, Resting HR [b.min−1] 72.7 ± 5.57 65.0–83.0
and interspersed by 1 min of active recovery at 70 % VO2max [ml.kg−1.min−1] 27.8 ± 5.69 19.3–37.0
HRmax. This protocol was repeated in the first three train-
BMI body mass index, SBP systolic blood pressure, DBP diastolic
ing sessions. The last three training sessions consisted of blood pressure, HR heart rate, b.min−1 beats per minute, VO2max max-
15 × 1-min bouts at 90–95 % HRmax interspersed by a min- imum aerobic capacity
ute active recovery at 70 % HRmax. Each training session
was ended by a 5-min cool-down at 50 % HRmax. There-
fore, a total of 30-min duration was spent in each session of 135 Pre
exercise for the first half of the intervention, while 40 min Post
was spent in the second half with warm-up and cool-down 130
Detraining
inclusive. 125
All the tests and measurements were repeated between
SBP [mmHg]

24 and 48 h after the last HIIT session. Participants were 120

then asked to refrain from any form of structured exercise
for 2 weeks and then return to the laboratory for a repeat of 115
all the assessments.
110

Statistical analysis 105

Descriptive statistics were calculated as means and stand- 100

ard deviations (SD). The differences in means of PEH fol-
lowing the maximal exercise capacity tests were compared
by single-factor analysis of variance (ANOVA). The three
tests and time intervals were independent factors with the
interaction effect (test × time) the dependent factor. The
level of significance was set at p < 0.05 for all analysis.
Cohen’s effect size (d) was calculated to compare the mag-
nitude of change in BP during recovery among the three
testing sessions (Cohen 1992). The PEH response was con-
sidered clinically significant if the BP dropped ≥3 mmHg
(Touyz et al. 2004).
Results
Twenty women completed the study. Table 1 summarizes
the physical and physiological characteristics of the partici-
pants. The women’s aerobic fitness levels were classified as
fair (VO2max: 25–33 ml kg−1 min−1) according to the norms
of Hoffman (2006).
There were no statistically significant differences in
mean SBP during 60 min recovery period after the pre-,
post- and detraining tests (pre: 118.6 ± 9.7 mmHg; post:
10 20 30 40 50 60
Time (min)
Fig. 1  Absolute change in SBP during recovery after the maximal
exercise capacity tests
118.8 ± 11.4 mmHg; detraining: 122.0 ± 11.4 mmHg;
p > 0.05), even though the detraining values were con-
sistently higher compared to pre- and post-training values
(Fig. 1). On all the three occasions, there were statistically
significant decreases in SBP over 60 min (p < 0.001); how-
ever, the interaction effect (test × time) was not statistically
significant (p > 0.05).
The magnitude of the change in SBP during recovery
after the maximal exercise capacity tests was statistically
significant at each assessment. Figure 2 indicates that SBP
was lowered by 10.13 mmHg (7.76 %, p < 0.001) after the
baseline assessment, by 11.11 mmHg (8.84 %; p < 0.001)
after the HIIT intervention and by 10.2 mmHg (7.84 %;
p < 0.001) after detraining. However, the magnitudes of
these changes were not statistically significantly differ-
ent between assessments (p > 0.05). The effect sizes (ES)
analysis also indicated only trivial practically significant

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80 Eur J Appl Physiol (2016) 116:77–84

0 86 Pre
84 Post
-2
%Change in SBP over 60 min

82 Detraining
-4 80

DBP [mmHg]
78
-6
76

74
-8
72
-10 70
ES=0.12 ES=0.12†

ES=0.01 68
-12
Pre Post Detraining 66
10 20 30 40 50 60
Fig. 2  Relative change in SBP over 60 min after maximal exercise Time [min]
capacity tests. † Trivial practically significant effect between tests
Fig. 4  Absolute change in DBP during recovery after the maximal
exercise capacity tests
10 Pre
Post
Absolute change from resting

8
0
6
Detraining
SBP [mmHg]

-2
%Change in DBP over 60 min

2
-4
0

-2 -6
-4
¥ -8
-6
10 20 30 40 50 60 ES=0.22₴
Time [min] -10
ES=0.49₴
Fig. 3  Magnitude of the PEH response in SBP relative to resting -12 ES=0.61ᵯ
SBP. ¥ Clinically significant (>3 mmHg)
Pre Post Detraining

differences in the training and detraining effects of HIIT on Fig. 5  Relative change in DBP over 60 min after maximal exercise
capacity tests. Small practically significant effect between tests;
BP recovery after maximal exercise.
moderate practically significant effect between tests
The magnitude of the systolic hypotensive responses
were slightly greater after HIIT compared to pre-training
(5.04 vs. 4.28 mmHg) and both would be considered clini- DBP during recovery following all tests (p < 0.001); how-
cally significant (>3 mmHg decrease) (Fig. 3). This hypo- ever, the interaction (test × time) effect was not statistically
tensive response was reached between 25 and 35 min after significant (p = 0.06).
cessation of exercise. The PEH response after the detrain- Figure 5 illustrates that the change in DBP during
ing period was only 1.08 mmHg lower than resting values recovery was least after the pre-training test (4.25 mmHg;
and was only reached after approximately 55 min. 4.82 %; p = 0.04), followed by post-training assessment
No statistically significant differences in mean DBP (5.72 mmHg; 7.13 %; p < 0.001). The decrease in DBP
over the 60 min recovery period were observed after the during recovery was most pronounced after the detraining
maximal exercise tests (pre: 77.5 ± 6.1 mmHg; post: assessment (8.0 mmHg; 9.63 %; p < 0.001). The differ-
76.9 ± 6.0 mmHg; detraining: 78.1 ± 6.8 mmHg; p > 0.05) ences in the magnitudes of the changes were not statisti-
(Fig. 4). There was a statistically significant time effect for cally significant among tests periods (p > 0.05); however,

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Eur J Appl Physiol (2016) 116:77–84
these differences were classified as small to moderately
practically significant (ES = 0.22–0.61).
After 60 min recovery, DBP were 2.33 mmHg (pre-
training), 4.26 mmHg (post-training), and 3.87 mmHg
(detraining) lower compared to resting DBP. The magni-
tude of the PEH response in DBP was considered clinically
significant (>3 mmHg) after HIIT and the detraining period
but not at pre-training. The hypotensive effect was reached
between 20- and 35-min post-exercise (see Fig. 6).
Discussion
The main finding of the study was that six HIIT sessions
resulted in a significant reduction in BP after an incre-
mental exercise test to exhaustion. However, after 2 weeks
of detraining, BP returned to near resting values. To our
knowledge, this study is the first to describe the PEH
response in young women following HIIT.
A high SBP used to be regarded less dangerous in terms
of future cardiovascular disease than high DBP, but now
elevated SBP alone has gained recognition as an important
cardiovascular risk factor (Kaplan 2000). Kaplan (2000)
contended that such effect can be attributed to the widen-
ing pulse pressure due to atherosclerotic stiffening of the
aorta and large capacitance vessels. This invariably pro-
vides a smaller rigid reservoir raising the systolic inflow
pressure and lowering diastolic pressures to a higher degree
than occurs with more flexible vessels. Thus, it has been
5
Pre
4 Post
3 Detraining
Absolute change from resting
2 et al. (2002) highlighted that a reduction in BP was associ-
DBP [mmHg]
1
0 fore possible that these hemodynamic functions may have
-1
-2
-3
-4
-5
10 20 30 40 50 60
Time [min]
Fig. 6  Magnitude of PEH response in DBP relative to resting DBP. ¥
Clinically significant (>3 mmHg)
81
reported that individuals with only high SBP have higher
risks for cardiovascular disease than those with high DBP
alone (Kannel 1999; Pescatello et al. 2004). Moreover, SBP
is known to increase all through adult life as age progresses
exposing one to the risk of developing hypertension. This
therefore explains reasons for the importance of the PEH
response, as it provides an effective lowering of BP which
will serve as a protective mechanism against cardiovascular
risk and the development of cardiovascular disease.
The magnitude of PEH in terms of SBP following the
maximal exercise capacity test in the present study was
significantly greater after the training intervention than pre-
training (−5.04 vs. −4.58 mmHg), but 2 weeks detraining
caused the effect to disappear as the hypotensive response
was reduced to 1.08 mmHg. DBP observed post-training
was also significantly lowered by 4.3 mmHg which was
greater compared to pre-training changes (−2.3 mmHg).
This clinically significant effect (−3.5 mmHg) was sus-
tained after detraining. Similar to the current study, Mer-
edith et al. (1990) found BP reductions of 8 mmHg in SBP
and 5 mmHg in DBP after 4 weeks of cycling exercise at
60–70 % VO2max in normotensive men; however, after
2 weeks of detraining, SBP returned to baseline values.
Meredith et al. (1990) upon analysis of the hemodynamic
responses showed that total peripheral resistance (TPR)
was significantly lower after training but increased after
detraining to baseline values. This may suggest that TPR
may have contributed to the reduction in BP after the exer-
cise intervention, as the reverse occurred after detraining.
Even though hemodynamic variables were not assessed in
the current study, it is possible that the observed reduction
in BP after training may have caused a decreased sympa-
thetic vasoconstrictor nerve activity outflow to the vascular
beds of the active skeletal muscles and then the arterial and
baroreflex are reset to a lower BP than initial levels before
exercise (Floras et al. 1989). Moreover, Brandão Rondon
ated with a reduction in left ventricular end-diastolic vol-
ume and a consistent decrease in SV and HR. It is there-
reversed with detraining to increase BP again to baseline
values. Millen et al. (2013) reported a significant reduc-
tion of 8 mmHg in both SBP and DBP following similar
training methods as in this study. Their intervention lasted
6 weeks of cycling exercise and involved overweight or
obese hypertensive middle-aged adults. Considering that
¥
¥
resting BP is a major predictor of the magnitude of PEH
(Cardoso et al. 2010), the difference in results is not sur-
prising. The observed difference in magnitude of PEH
compared to this study can be attributed to the difference
in study populations (older vs. younger adults) and BP sta-
tus (pre-hypertensive and hypertensive vs. normotensive).
Moreover, the length of the interventions in the study by
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82
Millen et al. (2013) as well as the duration of the exercise
bouts could have further contributed to the difference in
results, since the magnitude of PEH may also be affected
by the duration of exercise (Bennett et al. 1984).
Forjaz et al. (1998) reported significant but similar
reductions in BP after 45 min of exercise performed at
varying intensities of 30, 50, and 70 % VO2max in young
normotensive individuals. Since intensity of exercise plays
a role in the hemodynamic, thermoregulatory, and neural
responses during exercise, differences in the magnitude of
the PEH responses were expected. However, Forjaz et al.
(1998) found similar responses among the varying intensi-
ties of exercise and it cannot be explained why the response
observed after the higher intensity exercise (70 % VO2max)
was not significantly higher than for intensities at 30 and
50 % VO2max. Perhaps the exercise at 70 % VO2max relative
to 30 and 50 % VO2max was not intense enough to cause a
significant difference in magnitude of PEH in normotensive
individuals, as compared to the current study (90–95 %
VO2max).
In contrast, Piepoli et al. (1994) found that maximal
exercise but not light exercise caused PEH in young normo-
tensive individuals. These authors did not specify the exact
intensity in terms of VO2max or HRmax, but it is believed that
the difference in intensity was wide enough to cause a sig-
nificant difference in PEH. Similarly, Hagberg et al. (1987)
showed that the hypotensive response was greater after
exercise at 70 % VO2max than exercise performed at 50 %
VO2max in older, hypertensive subjects. It is clear that the
difference in population of the two studies in terms of age
and hypertension may have accounted for the difference in
results, as older hypertensives have high resting BP. It is
well known that the PEH response after any type of exer-
cise is greater in hypertensive than normotensive individu-
als (Kenney and Seals 1993).
Previous studies (Chan and Burns 2013; Ciolac et al.
2010; Cote et al. 2014; Liu et al. 2012; Nybo et al. 2010;
Rossow et al. 2010) have used similar intensity of training
and have found significant reductions in BP following high-
intensity training, but unfortunately they did not include a
detraining component to compare the current results with.
Thus, to our knowledge, this is the first study to describe
the training and detraining effects of a short-term HIIT
intervention. Future studies could assess whether long-
term training (>4 weeks) will have a change in the training
response that will be sustained after weeks of detraining or
be reversed completely as was found in this study.
The findings suggest that the magnitude of the PEH
response is possibly related to exercise intensity, i.e., the
higher the exercise intensity, the greater the PEH response.
However, more studies should be conducted in at risk pop-
ulations (hypertensive and overweight/obese) where the
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Eur J Appl Physiol (2016) 116:77–84
exercise intensity is carefully quantified before conclusive
affirmations can be made.
Study limitations
BP measurements after detraining was only taken after the
maximal exercise capacity test and not before, which would
have reflected the direct effect of HIIT only without any
additional exercise (i.e., the maximal exercise capacity can
be considered an extra exercise session). For this reason,
the effect of detraining on PEH was only compared fol-
lowing the maximal exercise capacity tests. Thus, in future
research, BP monitoring can be done on the day follow-
ing the detraining period to better compare the detraining
and the training effects. Furthermore, future studies should
consider monitoring the dynamics of the changes in blood
pressure for longer than 1 h after exercise and possibly also
during free-living conditions.
Conclusion
This study showed that six sessions of HIIT is associated
with clinically significant PEH responses in overweight/
obese young women, but 2 weeks of detraining reversed
the training effects such that SBP returned near to resting
values. However, DBP was not affected by detraining as it
remained consistently lower and the magnitude remained
clinically significant. Therefore, it is important that regular
exercise training be encouraged, so that the acquired ben-
efits would be sustained.
Acknowledgments We are grateful to the volunteers who sacri-
ficed their time out from their busy schedules, their interest, and com-
mitment in this study. This research was supported by a grant from
Kwame Nkrumah University of Science and Technology. Biggie
Bonsu is currently at the Department of Sports and Exercise Science,
Faculty of Allied Health Sciences, Kwame Nkrumah University of
Science and Technology, Kumasi Ghana.
Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict
of interest.
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