Exercise 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 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[Combining Dot Above]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[Combining Dot Above]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 aerobic exercise. Several reports directly comparing high-intensity interval exercise with submaximal constant-load exercise indicate 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 exercise (15,23,24). Therefore, published evidence to date is insufficient 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 submaximal constant-load exercise. On the basis of studies reporting 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.
Experimental Approach to the Problem
To test our hypothesis, we had subjects perform, in random sequence on separate days, 1 nonexercise control trial, one 30-minute submaximal constant-load exercise session, and 2 commonly used high-intensity interval exercise routines. One interval exercise routine (aerobic interval exercise [AIE]) consisted of four 4-minute intervals at >90% maximum heart rate (HRmax) separated by 3 minutes of active recovery (20,33). The other interval exercise routine (sprint interval exercise, SIE) consisted of 6 “all-out” 30-second sprints, separated by 4 minutes of active recovery (i.e., Wingate tests) (4,11,27).
Thirteen (12 males, 1 female) healthy nonsmoking young adults (age range 19–28) participated in this study. The study was approved by the Arizona State University institutional review board, and written informed consent was obtained from all subjects as per the Declaration of Helsinki. Subjects were screened using the Physical Activity Readiness Questionnaire (PAR-Q) and were excluded if they answered “yes” to any of the questions in the PAR-Q. None of the subjects were taking antihypertensive or vasoactive medications/supplements. Subjects were instructed to avoid caffeine consumption for ≥12 hours before baseline testing and exercise visits.
After the initial screening, subjects reported to the laboratory at 1,200 hours on a separate day, 4 hours after eating breakfast. Subjects then underwent baseline anthropometric assessment. Height was measured using a stadiometer, and subjects were weighed using a Detecto balance beam scale (Webb City, MO, USA). Body composition was measured using air displacement plethysmography (BodPod, Life Measurement 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, Waukesha, WI, USA) (Table 1). All research activities were conducted in a thermoneutral environment (≈22–23° C).
Subjects then underwent a maximal graded exercise test (GXT) on an Ergoline VIAsprint 150P Bitz cycle ergometer (Bitz, Germany). After 2 minutes of unloaded cycling, resistance was increased by 25 W·min−1 (men) or by 20 W·min−1 (woman) until volitional fatigue. Ventilation and gas exchange were monitored continuously with a portable indirect calorimetry system (Oxycon Mobile, Carefusion, San Diego, CA, USA), which was calibrated before every exercise test as per the manufacturer's specifications. Heart rate was continuously monitored using a Polar heart rate monitor (Lake Success, NY, USA). Maximum heart rate during the GXT was recorded and used to determine exercise intensity for the continuous and AIE conditions.
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 × subject weight (in kilograms). All exercise was performed on a Monark 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. Their data were excluded from all analyses.
After exercise, BP was measured every 15 minutes for 3 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 laboratory. Subjects were provided ad libitum access to drinking water for the duration of each visit, although no subject consumed more than 500 ml during any visit. Finally, all BP measurements were carried out with subjects comfortably seated upright to minimize confounding due to posture.
Data are expressed as mean ± SD. All p values were calculated assuming 2-tailed alternate hypothesis; p ≤ 0.05 was considered statistically significant. Linear mixed models were used to detect overall and hourly differences in BP data between the 4 trials (28). The analysis was conducted in a hierarchical fashion using the restricted maximum likelihood model. Both fixed and random effects were explored in the model. The “variance components” covariance error structure was used for examining random effects in the model (30,31). Trial condition, baseline BP, and time were used as fixed effects, and time was used as random effect to account for interindividual and diurnal variations in BP. Further addition of height, weight, percent body fat, and V[Combining Dot Above]O2peak did not improve model fit, and therefore, these variables were not included as covariates in the analysis. Post hoc analysis was performed using the Bonferroni adjustment for multiple comparisons. Systolic BP (SBP) and diastolic BP (DBP) were analyzed separately. One-way analysis of variance was used to test for differences in baseline BP values between the 4 trials. The SPSS software (SPSS 20.0; IBM Corp., Armonk, NY, USA) was used for all statistical analyses.
Postexercise Systolic Blood Pressure
There were no significant differences in baseline SBP values between the 4 conditions (Table 2).
Postexercise hypotension was observed for SBP after each exercise trial (Figure 1A), with a peak decrease observed at 1-hour postexercise. All 3 exercise conditions significantly reduced SBP compared with control in the first- and second-hour postexercise. During the second-hour postexercise, SBP after AIE was 4–5 mm Hg lower than both SSE and SIE. During the third-hour postexercise, SBP after AIE was significantly lower than both control and SSE conditions by 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.
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 exercise produce similar PEH need to be interpreted with caution. This underscores the need for extending the postexercise 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 previous 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[Combining Dot Above]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 reduction and therefore is not necessary to maximize PEH. However, 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. 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[Combining Dot Above]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 minutes of continuous or accumulated activity at 40–60% of V[Combining Dot Above]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 reduction 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 exercise that reported BP at time points up to 1 hour postexercise (18,27,29). Furthermore, the PEH was largely complete by 3-hour postexercise (with the exception of DBP after AIE). Conducting experiments in a laboratory environment 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 consumed 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 maximize 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.
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 augmenting BP control.
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.
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