POSTEXERCISE HYPOTENSION AFTER CONTINUOUS,
AEROBIC INTERVAL, AND SPRINT INTERVAL EXERCISE
SIDDHARTHA S. ANGADI,1 DHARINI M. BHAMMAR,2
1
Healthy Lifestyles Research Center, School of Nutrition and Health Promotion, Arizona State University, Phoenix, Arizona;
and 2Department of Internal Medicine, Pulmonary and Critical Care Medicine Unit, Institute for Exercise and Environmental
Medicine, Texas Health Presbyterian Hospital, University of Texas Southwestern Medical Center, Dallas, Texas
ABSTRACT
Angadi, SS, Bhammar, DM, and Gaesser, GA. Postexercise
hypotension after continuous, aerobic interval, and sprint interval
exercise. J Strength Cond Res 29(10): 2888–2893, 2015—We
examined the effects of 3 exercise bouts, differing markedly in
intensity, on postexercise hypotension (PEH). Eleven young adults
(age: 24.6 6 3.7 years) completed 4 randomly assigned experi-
mental conditions: (a) control, (b) 30-minute steady-state exercise
(SSE) at 75–80% maximum heart rate (HRmax), (4) aerobic inter-
val exercise (AIE): four 4-minute bouts at 90–95% HRmax, sepa-
rated by 3 minutes of active recovery, and (d) sprint interval
exercise (SIE): six 30-second Wingate sprints, separated by 4 mi-
nutes of active recovery. Exercise was performed on a cycle
ergometer. Blood pressure (BP) was measured before exercise
and every 15-minute postexercise for 3 hours. Linear mixed models
were used to compare BP between trials. During the 3-hour post-
exercise, systolic BP (SBP) was lower (p , 0.001) after AIE
(118 6 10 mm Hg), SSE (121 6 10 mm Hg), and SIE (121 6
11 mm Hg) compared with control (124 6 8 mm Hg). Diastolic
BP (DBP) was also lower (p , 0.001) after AIE (66 6 7 mm
Hg), SSE (69 6 6 mm Hg), and SIE (68 6 8 mm Hg) compared
with control (71 6 7 mm Hg). Only AIE resulted in sustained
(.2 hours) PEH, with SBP (120 6 9 mm Hg) and DBP (68 6
7 mm Hg) during the third-hour postexercise being lower (p #
0.05) than control (124 6 8 and 70 6 7 mm Hg). Although all
exercise bouts produced similar reductions in BP at 1-hour
postexercise, the duration of PEH was greatest after AIE.
KEY WORDS Wingate, blood pressure, high-intensity exercise
INTRODUCTION
E
xercise is a valuable therapeutic adjunct for
improving blood pressure (BP) control (22). Both
acute exercise bouts and chronic exercise training
have been shown to lower BP significantly in
Address correspondence to Siddhartha S. Angadi, sangadi@asu.edu.
29(10)/2888–2893
Journal of Strength and Conditioning Research
Ó 2015 National Strength and Conditioning Association
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2888 Journal of Strength and Conditioning Research
Copyright © National Strength and Conditioning Association Unauthorized reproduction of this article is prohibited.
AND GLENN A. GAESSER1
a variety of populations (6,22). Most studies indicate that
exercise intensity is not an important predictor of the BP
reduction after exercise training (8) or after an acute bout
of submaximal constant-load exercise (7,9,13,14,19,23,24).
However, these studies used submaximal continuous aerobic
exercise at intensities between approximately 30 and 75% of
either maximum heart rate or V_ O2.
It is unclear, for acute exercise, whether very high intensities,
such as those attained in high-intensity interval exercise, would
produce a greater postexercise hypotension (PEH). Incremental
maximal exercise to volitional fatigue has been shown to
produce a greater PEH than constant-load exercise at 40 and
60% of V _ O2max (7). Thus, it could be hypothesized that high-
intensity interval exercise that elicits maximal or near-maximal
intensities might produce a greater PEH than continuous aero-
bic exercise. Several reports directly comparing high-intensity
interval exercise with submaximal constant-load exercise indi-
cate no difference in PEH (5,18,27,29). However, 3 of these
studies measured PEH for only 60-minute postexercise
(18,27,29), whereas the fourth study measured only 24-hour
ambulatory BP and did not report acute hourly BP (5).
Postexercise hypotension can last longer than 60 minutes
(13,16,19,24) and higher-intensity exercise may result in
a more prolonged PEH compared with lower-intensity exer-
cise (15,23,24). Therefore, published evidence to date is insuf-
ficient to determine whether the PEH after high-intensity
interval exercise differs from that after submaximal constant-
load exercise beyond the initial 60-minutes postexercise.
Because of the increasing interest in health benefits of high-
intensity interval exercise training (10,12), our specific aim was
to compare PEH after high-intensity interval exercise and sub-
maximal constant-load exercise. On the basis of studies report-
ing a more pronounced PEH after incremental exercise to
volitional fatigue (7), and a more sustained PEH after higher-
intensity exercise (15,24), we hypothesized that high-intensity
interval exercise would elicit a PEH of greater magnitude and
duration compared with submaximal constant-load exercise.
METHODS
Experimental Approach to the Problem
To test our hypothesis, we had subjects perform, in random
sequence on separate days, 1 nonexercise control trial, one
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Journal of Strength and Conditioning Research | www.nsca.com

were screened using the Physical Activity Readiness Question-

naire (PAR-Q) and were excluded if they answered “yes” to
TABLE 1. Descriptive characteristics (N = 11).
any of the questions in the PAR-Q. None of the subjects were
Sex (men/women) 10/1 taking antihypertensive or vasoactive medications/supple-
ments. Subjects were instructed to avoid caffeine consumption
Age (y) 24.6 6 3.7
for $12 hours before baseline testing and exercise visits.
Height (cm) 169.9 6 7.2
Weight (kg) 69.8 6 12.6 Procedures
Body fat (%) 14.2 6 4.8
After the initial screening, subjects reported to the laboratory
V_ O2peak (ml$kg21$min21) 48.1 6 9.2
Resting SBP (mm Hg) 122 6 11 at 1,200 hours on a separate day, 4 hours after eating
Resting DBP (mm Hg) 68 6 7 breakfast. Subjects then underwent baseline anthropometric
Resting heart rate (b$min21) 61 6 8 assessment. Height was measured using a stadiometer, and
Peak heart rate (b$min21) 182 6 8 subjects were weighed using a Detecto balance beam scale
(Webb City, MO, USA). Body composition was measured
using air displacement plethysmography (BodPod, Life Mea-
surement Inc., Concord, CA, USA). Subjects then rested for
15 minutes, and baseline BP and heart rate were measured
using a Dinamap oscillometric BP monitor (GE Healthcare,
30-minute submaximal constant-load exercise session, and 2
Waukesha, WI, USA) (Table 1). All research activities were
commonly used high-intensity interval exercise routines.
conducted in a thermoneutral environment (z22–238 C).
One interval exercise routine (aerobic interval exercise
Subjects then underwent a maximal graded exercise test
[AIE]) consisted of four 4-minute intervals at .90% maxi-
(GXT) on an Ergoline VIAsprint 150P Bitz cycle ergometer
mum heart rate (HRmax) separated by 3 minutes of active
(Bitz, Germany). After 2 minutes of unloaded cycling, resistance
recovery (20,33). The other interval exercise routine (sprint
was increased by 25 W$min21 (men) or by 20 W$min21
interval exercise, SIE) consisted of 6 “all-out” 30-second
(woman) until volitional fatigue. Ventilation and gas exchange
sprints, separated by 4 minutes of active recovery (i.e., Wing-
were monitored continuously with a portable indirect calorim-
ate tests) (4,11,27).
etry system (Oxycon Mobile, Carefusion, San Diego, CA, USA),
Subjects which was calibrated before every exercise test as per the man-
Thirteen (12 males, 1 female) healthy nonsmoking young ufacturer’s specifications. Heart rate was continuously moni-
adults (age range 19–28) participated in this study. The study tored using a Polar heart rate monitor (Lake Success, NY,
was approved by the Arizona State University institutional USA). Maximum heart rate during the GXT was recorded
review board, and written informed consent was obtained and used to determine exercise intensity for the continuous
from all subjects as per the Declaration of Helsinki. Subjects and AIE conditions.

TABLE 2. Baseline, overall, and hourly postexercise systolic and DBP for control, SSE, AIE, and SIE.*

Control SSE SIE AIE p

SBP (mm Hg)

Baseline 119 6 9 124 6 12 121 6 11 124 6 11 0.713
Overall (3 h) 124 6 8 121 6 10† 121 6 11† 118 6 10† ,0.001
First hour 124 6 8 118 6 10† 120 6 11† 118 6 11† ,0.001
Second hour 123 6 8 119 6 8† 120 6 11† 115 6 8†z§ ,0.001
Third hour 124 6 8 125 6 10 123 6 10 120 6 9†z ,0.001
DBP (mm Hg)
Baseline 66 6 7 67 6 6 69 6 6 68 6 9 0.707
Overall (3 h) 71 6 7 69 6 6† 68 6 8† 66 6 7†z ,0.001
First hour 71 6 7 66 6 5† 66 6 7† 66 6 8† ,0.001
Second hour 70 6 7 68 6 5 67 6 8† 66 6 5† ,0.001
Third hour 70 6 7 72 6 7 70 6 8 68 6 7†z§ ,0.001

*DBP = diastolic BP; BP = blood pressure; SSE = steady-state exercise; AIE = aerobic interval exercise; SIE = sprint interval
exercise; SBP = systolic BP.
†Significantly lower than control.
zSignificantly lower than SSE.
§Significantly lower than SIE.

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 Exercise Intensity and Blood Pressure

After the baseline graded maximal exercise test, subjects

were assigned to a randomized sequence of 4 visits that
included a control condition and 3 exercise trials. Each of
these trials was performed on different days and separated by
.1 week to minimize confounding by carryover effects. All
visits were carried out at the same time of day to minimize
effects of diurnal variation. Subjects reported to the laboratory
at 1,200 hours for each trial, 4 hours after eating a breakfast
meal. The breakfast meal was of the subject’s choosing but
was the same within each subject for all 4 trials. Subjects rested
for 15 minutes in a seated position before resting BP was
recorded. Two separate readings 5 minutes apart were taken,
and the average of both values was used as the resting BP.
The 3 exercise conditions consisted of (a) steady-state
exercise (SSE): 30 minutes of uninterrupted exercise at a work
rate that elicited 75–80% HRmax; (b) AIE: four 4-minute
bouts at 90–95% HRmax, separated by 3 minutes of active
recovery at 50% HRmax, and (c) sprint interval exercise (SIE):
six 30-second “all-out” Wingate sprints, separated by 4 minutes
of active recovery at 50% HRmax. Resistance on the cycle
ergometer for the Wingate tests was set at 0.075 3 subject
weight (in kilograms). All exercise was performed on a Mon-
ark Ergomedic 828E friction-braked cycle ergometer (Dalarna,
Sweden). Each exercise condition included a 10-minute
warm-up and a 5-minute cooldown at a work rate associated
with 50% HRmax. We did not observe any adverse events
during SSE or AIE. Two subjects dropped out of the study
after experiencing vasovagal events during the SIE condition.
Figure 1. Systolic (A) and diastolic (B) blood pressure (BP) during
Their data were excluded from all analyses. 3 hours of resting control and after 30 minutes of steady-state exercise
After exercise, BP was measured every 15 minutes for 3 (SSE), sprint interval exercise (SIE), and aerobic interval exercise (AIE).
hours using Dinamap BP monitor. For each measurement
time point, the mean of 2 readings taken 5 minutes apart was
used. During the control condition, subjects rested quietly in
a seated position for the entire duration of the study in the V_ O2peak did not improve model fit, and therefore, these
laboratory. Subjects were provided ad libitum access to variables were not included as covariates in the analysis. Post
drinking water for the duration of each visit, although no hoc analysis was performed using the Bonferroni adjustment
subject consumed more than 500 ml during any visit. Finally, for multiple comparisons. Systolic BP (SBP) and diastolic BP
all BP measurements were carried out with subjects com- (DBP) were analyzed separately. One-way analysis of vari-
fortably seated upright to minimize confounding due to ance was used to test for differences in baseline BP values
posture. between the 4 trials. The SPSS software (SPSS 20.0; IBM
Corp., Armonk, NY, USA) was used for all statistical
Statistical Analyses analyses.
Data are expressed as mean 6 SD. All p values were calcu-
lated assuming 2-tailed alternate hypothesis; p # 0.05 was RESULTS
considered statistically significant. Linear mixed models Postexercise Systolic Blood Pressure
were used to detect overall and hourly differences in BP data There were no significant differences in baseline SBP values
between the 4 trials (28). The analysis was conducted in between the 4 conditions (Table 2).
a hierarchical fashion using the restricted maximum likeli- Postexercise hypotension was observed for SBP after each
hood model. Both fixed and random effects were explored in exercise trial (Figure 1A), with a peak decrease observed at
the model. The “variance components” covariance error 1-hour postexercise. All 3 exercise conditions significantly
structure was used for examining random effects in the reduced SBP compared with control in the first- and
model (30,31). Trial condition, baseline BP, and time were second-hour postexercise. During the second-hour postexer-
used as fixed effects, and time was used as random effect to cise, SBP after AIE was 4–5 mm Hg lower than both SSE and
account for interindividual and diurnal variations in BP. SIE. During the third-hour postexercise, SBP after AIE was
Further addition of height, weight, percent body fat, and significantly lower than both control and SSE conditions by
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2890 Journal of Strength and Conditioning Research

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4–5 mm Hg, and only AIE resulted in SBP lower than control
during the third-hour postexercise (Table 2).
Postexercise Diastolic Blood Pressure
There were no significant differences in baseline DBP values
between the 4 conditions (Table 2). Overall, DBP during the
3-hour postexercise period after AIE, SSE, and SIE was
significantly lower than the control condition (Table 2). In
addition, average DBP during the 3-hour postexercise period
after AIE was significantly lower than after SSE.
Postexercise hypotension was observed for DBP after each
exercise condition (Figure 1B), with a peak decrease during the
first-hour postexercise. Compared with the control condition,
during the first-hour postexercise, all 3 exercise conditions
reduced DBP by 5 mm Hg (Table 2). In the second-hour
postexercise, DBP was lower than control only for AIE
(4 mm Hg lower) and SSE (3 mm Hg lower). During the
third-hour postexercise, DBP after AIE was significantly lower
by 2–4 mm Hg compared with all other conditions.
DISCUSSION
The primary findings of our investigation are that only AIE
produced a significantly greater magnitude of PEH than SSE
for overall DBP, and only AIE produced a significantly
longer duration of PEH than SSE, with reductions in SBP
and DBP lasting up to 3 hours. Our findings also suggest that
the conclusions of previous studies, which showed that high-
intensity interval exercise and submaximal continuous exer-
cise produce similar PEH need to be interpreted with
caution. This underscores the need for extending the post-
exercise measurement of BP beyond the first hour. Similar to
previous reports (18,27,29), all 3 exercise conditions in our
study elicited similar PEH during the first-hour postexercise
(Figure 1 and Table 2). However, only AIE produced a PEH
that was significantly lower than the control trial during each
hour of the 3-hour postexercise period. Had our study only
measured BP for 1-hour postexercise, as was done in pre-
vious studies comparing high-intensity interval exercise with
continuous exercise (18,27,29), our results would essentially
confirm those findings. However, it is apparent that AIE has
a more potent protracted influence on PEH than either SSE
or SIE and lasts approximately 3 hours for SBP (Figure 1A)
and at least 3 hours for DBP (Figure 1B).
The results of the AIE trial support previous findings that
showed a greater PEH after a maximal incremental exercise
test compared with submaximal continuous exercise at
either 40 or 60% of V_ O2peak (7). The results of the SIE trial
suggest that supramaximal exercise (e.g., 30-second Wingate
tests) does not provide an additional stimulus for BP reduc-
tion and therefore is not necessary to maximize PEH. How-
ever, it is important to note that short-duration (6 second)
Wingate-based exercise training has been demonstrated to
improve BP outcomes in elderly adults (1).
Two of 13 subjects dropped out of the study after
experiencing vasovagal events during the SIE condition.
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Journal of Strength and Conditioning Research | www.nsca.com
This highlights the relative safety of AIE as compared with
SIE. In addition, AIE has been shown to be well tolerated in
a number of populations, including coronary heart disease,
metabolic syndrome, and heart failure (2,25,26,36). These
high intensities are well tolerated especially when based on
baseline V_ O2peak assessments before the intervention as was
done in this study. Finally, high-intensity interval exercise is
also safe (26) and has been reported to be more enjoyable
than continuous exercise (3). Nevertheless, for some clinical
populations, it may be advisable for participants to first
obtain physician approval and also engage only in medically
supervised exercise training (21).
Our findings also suggest that current ACSM exercise
guidelines for BP reduction (22) could be expanded to
include AIE exercise. Present guidelines recommend 30 mi-
nutes of continuous or accumulated activity at 40–60% of
V_ O2 reserve, and there is a substantial body of evidence to
support such a recommendation. However, high-intensity
interval exercise such as the AIE protocol used in this study
might offer a viable and attractive alternative to traditional
submaximal continuous exercise for optimal BP control.
Exercise training with the AIE protocol used in this study
has been shown to reduce BP more than SSE in some
(20,33), but not all studies (36). In general, high-intensity
interval exercise training reduces BP by at least much as
SSE (17) and may provide additional cardiovascular and
metabolic benefits (10,35).
Our study highlights the importance of using a control
trial for interpretation of the PEH response. This has not
always been done (27,29). Although the PEH response was
evident even when compared with the pre-exercise baseline
value for each exercise condition, due to the fact that both
SBP and DBP increased over 3 hours during the control
condition, the magnitude of the PEH was greater when
viewed from the perspective of comparing BP responses
after each exercise condition with those during the time-
matched 3-hour control period (Figure 1). An afternoon rise
in BP has been noted by some investigators (32,34). Even
during a 60-minute measurement period, Lacombe et al. (18)
documented a rise in resting BP during late afternoon in
their study of PEH. In our study, AIE elicited a peak reduc-
tion in SBP from baseline of 6–7 mm Hg during the second-
hour postexercise. Compared with the corresponding time
points during the control trial, however, the PEH after AIE
was 8–10 mm Hg (Figure 1A). This reduction is similar to
that reported by Lacombe et al. (18), who only monitored
BP for 1 hour postexercise. Our results suggest that this
reduction in BP after AIE persists for approximately 3 hours
postexercise, although the magnitude of the reduction wanes
during the third-hour postexercise.
This study has limitations as well as strengths. The
duration of postexercise BP measurement was relatively
short (3 hours) in comparison with studies using ambulatory
BP (7,13,23). It was, however, longer than all previous
studies comparing continuous and high-intensity interval
VOLUME 29 | NUMBER 10 | OCTOBER 2015 | 2891
 Exercise Intensity and Blood Pressure
exercise that reported BP at time points up to 1 hour post-
exercise (18,27,29). Furthermore, the PEH was largely com-
plete by 3-hour postexercise (with the exception of DBP
after AIE). Conducting experiments in a laboratory environ-
ment precluded direct application to free-living conditions.
However, our experimental protocol provided for well-
controlled measurements of BP (e.g., posture, time of day)
and eliminated confounding from environmental conditions,
including diet, physical activity, and temperature. Despite
having documented significant differences in PEH between
exercise conditions, we were unable to explore potential
mechanisms. Finally, we did not assess hydration status
before and during exercise. Although subjects consumed
water ad libitum in the postexercise period, no subject con-
sumed more than 500 ml during any visit.
In conclusion, SSE, AIE, and SIE produced similar overall
PEH during a 3-hour postexercise measurement period, with
the peak reduction in BP occurring approximately 1 hour
after exercise. However, the duration of the PEH was
greatest for AIE, and only AIE produced a PEH during
the third-hour postexercise. The fact that AIE was superior
to the largely anaerobic and exhaustive SIE suggests that
there may be an upper limit to exercise intensity, and that
extremely high-intensity exertion is not necessary to maxi-
mize PEH. Because of the increasing popularity of high-
intensity interval exercise training and support for its health
benefits (10), AIE may be a viable alternative to traditional
steady-state submaximal exercise for optimizing BP control.
PRACTICAL APPLICATIONS
Exercise is valuable adjunctive therapy for management of
BP, with single exercise bouts producing significant PEH
that may last several hours. Exercise intensity is not
important regarding the magnitude of the PEH immediately
after exercise, but beyond the first-hour postexercise, AIE
seems to be superior to less intense continuous exercise or
extremely intense sprint interval exercise for sustaining PEH.
Because AIE is well tolerated, it may be a viable alternative
to traditional steady-state submaximal exercise for augment-
ing BP control.
ACKNOWLEDGMENTS
The authors thank Ms. Cindy Furmanek and Mr. Dameon
Hahn for their assistance in data collection. No funding was
received for this research. No conflicts of interest to declare.
REFERENCES
1. Adamson, SB, Lorimer, R, Cobley, JN, and Babraj, JA. Extremely
short–duration high-intensity training substantially improves the
physical function and self-reported health status of elderly adults.
J Am Geriatr Soc. 62: 1380–1381, 2014.
2. Angadi, SS, Mookadam, F, Lee, CD, Tucker, WJ, Haykowsky, MJ,
and Gaesser, GA. High-intensity interval training vs. moderate-
intensity continuous exercise training in heart failure with preserved
ejection fraction: A pilot study. J Appl Physiol (1985)
jap.00518.02014, 2014.
the TM
2892 Journal of Strength and Conditioning Research
Copyright © National Strength and Conditioning Association Unauthorized reproduction of this article is prohibited.
3. Bartlett, JD, Close, GL, MacLaren, DP, Gregson, W, Drust, B, and
Morton, JP. High-intensity interval running is perceived to be more
enjoyable than moderate-intensity continuous exercise: Implications
for exercise adherence. J Sports Sci 29: 547–553, 2011.
4. Burns, SF, Oo, HH, and Anh Thanh Thuy, T. Effect of sprint
interval exercise on postexercise metabolism and blood pressure in
adolescents. Int J Sport Nutr Exerc Metab 22: 47–54, 2012.
5. Ciolac, EG, Guimaraes, GV, D’Avila, VM, Bortolotto, LA,
Doria, EL, and Bocchi, EA. Acute effects of continuous and
interval aerobic exercise on 24-h ambulatory blood pressure in
long-term treated hypertensive patients. Int J Cardiol 133:
381–387, 2009.
6. Cornelissen, VA and Fagard, RH. Effects of endurance training on
blood pressure, blood pressure-regulating mechanisms, and
cardiovascular risk factors. Hypertension 46: 667–675, 2005.
7. Eicher, JD, Maresh, CM, Tsongalis, GJ, Thompson, PD, and
Pescatello, LS. The additive blood pressure lowering effects of
exercise intensity on post-exercise hypotension. Am Heart J 160:
513–520, 2010.
8. Fagard, RH. Exercise is good for your blood pressure: Effects of
endurance training and resistance training. Clin Exp Pharmacol
Physiol 33: 853–856, 2006.
9. Forjaz, CL, Cardoso, CG Jr, Rezk, CC, Santaella, DF, and Tinucci, T.
Postexercise hypotension and hemodynamics: The role of exercise
intensity. J Sports Med Phys Fitness 44: 54–62, 2004.
10. Gaesser, GA and Angadi, SS. High-intensity interval training for
health and fitness: Can less be more? J Appl Physiol (1985) 111:
1540–1541, 2011.
11. Gibala, MJ and McGee, SL. Metabolic adaptations to short-term
high-intensity interval training: A little pain for a lot of gain? Exerc
Sport Sci Rev 36: 58–63, 2008.
12. Gillen, JB and Gibala, MJ. Is high-intensity interval training a time-
efficient exercise strategy to improve health and fitness? Appl Physiol
Nutr Metab 39: 409–412, 2013.
13. Guidry, MA, Blanchard, BE, Thompson, PD, Maresh, CM,
Seip, RL, Taylor, AL, and Pescatello, LS. The influence of short
and long duration on the blood pressure response to an acute
bout of dynamic exercise. Am Heart J 151: 1322.e5–1322.e12,
2006.
14. Jones, H, George, K, Edwards, B, and Atkinson, G. Is the magnitude
of acute post-exercise hypotension mediated by exercise intensity or
total work done? Eur J Appl Physiol 102: 33–40, 2007.
15. Keese, F, Farinatti, P, Pescatello, L, Cunha, FA, and Monteiro, WD.
Aerobic exercise intensity influences hypotension following
concurrent exercise sessions. Int J Sports Med 33: 148–153, 2012.
16. Keese, F, Farinatti, P, Pescatello, L, and Monteiro, W. A comparison
of the immediate effects of resistance, aerobic, and concurrent
exercise on postexercise hypotension. J Strength Cond Res 25: 1429–
1436, 2011.
17. Kessler, HS, Sisson, SB, and Short, KR. The potential for high-
intensity interval training to reduce cardiometabolic disease risk.
Sports Med 42: 489–509, 2012.
18. Lacombe, SP, Goodman, JM, Spragg, CM, Liu, S, and Thomas, SG.
Interval and continuous exercise elicit equivalent postexercise
hypotension in prehypertensive men, despite differences in
regulation. Appl Physiol Nutr Metab 36: 881–891, 2011.
19. MacDonald, JR. Potential causes, mechanisms, and implications of
post exercise hypotension. J Hum Hypertens 16: 225–236, 2002.
20. Molmen-Hansen, HE, Stolen, T, Tjonna, AE, Aamot, IL,
Ekeberg, IS, Tyldum, GA, Wisloff, U, Ingul, CB, and Stoylen, A.
Aerobic interval training reduces blood pressure and improves
myocardial function in hypertensive patients. Eur J Prev Cardiol 19:
151–160, 2012.
21. Pescatello, LS; American College of Sports Medicine. ACSM’s
Guidelines for Exercise Testing and Prescription. Philadelphia, PA:
Wolters Kluwer/Lippincott Williams & Wilkins Health, 2014.

22. Pescatello, LS, Franklin, BA, Fagard, R, Farquhar, WB, Kelley, GA,
and Ray, CA. Exercise and hypertension: American College of
Sports Medicine position stand. Med Sci Sports Exerc 36: 533–553,
2004.
23. Pescatello, LS, Guidry, MA, Blanchard, BE, Kerr, A, Taylor, AL,
Johnson, AN, Maresh, CM, Rodriguez, N, and Thompson, PD.
Exercise intensity alters postexercise hypotension. J Hypertens 22:
1881–1888, 2004.
24. Quinn, TJ. Twenty-four hour, ambulatory blood pressure responses
following acute exercise: Impact of exercise intensity. J Hum
Hypertens 14: 547–553, 2000.
25. Rognmo, Ø, Hetland, E, Helgerud, J, Hoff, J, and Slørdahl, SA. High
intensity aerobic interval exercise is superior to moderate intensity
exercise for increasing aerobic capacity in patients with coronary
artery disease. Eur J Cardiovasc Prev Rehabil 11: 216–222, 2004.
26. Rognmo, O, Moholdt, T, Bakken, H, Hole, T, Mølstad, P,
Myhr, NE, Grimsmo, J, and Wisløff, U. Cardiovascular risk of high-
versus moderate-intensity aerobic exercise in coronary heart disease
patients. Circulation 126: 1436–1440, 2012.
27. Rossow, L, Yan, H, Fahs, CA, Ranadive, SM, Agiovlasitis, S,
Wilund, KR, Baynard, T, and Fernhall, B. Postexercise hypotension
in an endurance-trained population of men and women following
high-intensity interval and steady-state cycling. Am J Hypertens 23:
358–367, 2010.
28. Schwartz, JE and Stone, AA. Strategies for analyzing ecological
momentary assessment data. Health Psychol 17: 6, 1998.
29. Scott, JM, Esch, BTA, McKenzie, DC, Koehle, MS, Sheel, AW, and
Warburton, DE. Post-exercise hypotension and cardiovascular
Copyright © National Strength and Conditioning Association Unauthorized reproduction of this article is prohibited.
the TM
Journal of Strength and Conditioning Research | www.nsca.com
responses to moderate orthostatic stress in endurance-trained males.
Appl Physiol Nutr Metab 33: 246–253, 2008.
30. Searle, SR, Casella, G, and McCulloch, CE. Variance Components.
Hoboken, NJ: John Wiley & Sons, 2009.
31. Singer, JD and Willett, JB. Applied Longitudinal Data Analysis:
Modeling Change and Event Occurrence. New York: Oxford University
Press, 2003.
32. Stergiou, GS, Vemmos, KN, Pliarchopoulou, KM, Synetos, AG,
Roussias, LG, and Mountokalakis, TD. Parallel morning and
evening surge in stroke onset, blood pressure, and physical activity.
Stroke 33: 1480–1486, 2002.
33. Tjonna, AE, Stolen, TO, Bye, A, Volden, M, Slordahl, SA, Odegard, R,
Skogvoll, E, and Wisloff, U. Aerobic interval training reduces
cardiovascular risk factors more than a multitreatment approach in
overweight adolescents. Clin Sci (Lond) 116: 317–326, 2009.
34. Wiinberg, N, Høegholm, A, Christensen, HR, Bang, LE,
Mikkelsen, KL, Nielsen, PE, Svendsen, TL, Kampmann, JP,
Madsen, NH, and Bentzon, MW. 24-h ambulatory blood pressure in
352 normal Danish subjects, related to age and gender. Am J
Hypertens 8: 978–986, 1995.
35. Wisløff, U, Ellingsen, Ø, and Kemi, OJ. High-intensity interval
training to maximize cardiac benefits of exercise training? Exerc
Sport Sci Rev 37: 139–146, 2009.
36. Wisløff, U, Støylen, A, Loennechen, JP, Bruvold, M, Rognmo, Ø,
Haram, PM, Tjønna, AE, Helgerud, J, Slørdahl, SA, and Lee, SJ.
Superior cardiovascular effect of aerobic interval training versus
moderate continuous training in heart failure patients a randomized
study. Circulation 115: 3086–3094, 2007.
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