Continuous and Accumulated Bouts of Cycling Matched by Intensity and Energy Expenditure Elicit Similar Acute Blood Pressure Reductions in Prehypertensive Men

Abstract

Fonseca, GF, Farinatti, PTV, Midgley, AW, Ferreira, A, de Paula, T, Monteiro, WD, and Cunha, FA. Continuous and accumulated bouts of cycling matched by intensity and energy expenditure elicit similar acute blood pressure reductions in prehypertensive men. J Strength Cond Res 32(3): 857–866, 2018—This study investigated differences in postexercise hypotension (PEH) after continuous vs. accumulated isocaloric bouts of cycling. Ten prehypertensive men, aged 23–34 years, performed 2 bouts of cycling at 75% oxygen uptake reserve, with total energy expenditures of 400 kcal per bout. One exercise bout was performed continuously (CONTIN) and the other as 2 smaller bouts each expending 200 kcal (INTER1 and INTER2). Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and cardiac autonomic control were monitored in a supine position for 10 minutes before and 60 minutes after each exercise bout, and during a control session. Compared with control, blood pressure was significantly reduced after CONTIN (SBP: ∆ − 3.4 mm Hg, p < 0.001; MAP: ∆ − 2.5 mm Hg, p = 0.001), INTER1 (SBP: ∆ − 2.2 mm Hg, p = 0.045), and INTER2 (SBP: ∆ − 4.4 mm Hg, p < 0.001; DBP: ∆ − 2.7 mm Hg, p = 0.045; MAP: ∆ − 3.3 mm Hg, p = 0.001). The PEH was similar in CONTIN and INTER2, whereas INTER2 elicited greater PEH than INTER1 (SBP and MAP: ∆ − 2.0 and ∆ − 1.8 mm Hg, respectively, p ≤ 0.05). Increases in sympathovagal balance from baseline were inversely related to changes in SBP and DBP after CONTIN and INTER2 (r = −0.64 to −0.71; p = 0.021–0.047). These findings indicate that similar amounts of PEH are observed when exercise is performed as a single 400-kcal exercise bout or 2 × 200-kcal bouts and that the exercise recovery pattern of cardiac autonomic activity may be important in eliciting PEH.

Introduction

Hypertension is a serious public health problem associated with increased risk of developing other cardiovascular diseases (CVDs) (³⁰), and the observation that 1 in 5 people with prehypertension tend to progress to hypertension within an average time frame of 4 years (⁴⁴) is of particular concern. Physical activity level also has been shown to be strongly associated with the development of CVD (⁶). Paffenbarger et al. (³¹), for example, showed that among 14,998 Harvard male alumni that initially presented without hypertension in 1962 or 1966, 681 (5%) developed hypertension by 1972, with those not engaging in vigorous sporting activities at 35% greater risk of developing hypertension than those who did. Regular physical exercise, especially aerobic exercise, has therefore often been recommended for the prevention, treatment, and control of hypertension (^36,41). Indeed, current evidence suggests that chronic reductions in blood pressure from engaging in long-term aerobic exercise programs are due largely to the summative effects of the blunted blood pressure response observed after single acute bouts of aerobic exercise (²³). These blunted responses occur for several hours after exercise compared with the immediate preexercise period, or a nonexercise control day, and is a phenomenon known as postexercise hypotension (PEH) (³⁷).

Although the optimal exercise prescription to maximize PEH remains unknown, research has established that the magnitude of PEH, and whether it occurs, largely depends on several basic components of exercise prescription such as intensity, duration, and mode (see ^{Ref. 35} for a review). Another component that has received less attention is whether the exercise is performed continuously or cumulatively. Some studies support the idea that accumulated bouts may be a better strategy for prescribing aerobic exercise, by providing greater PEH than continuous bouts (^2,5,22,32,33), whereas others suggested that continuous and accumulated acute exercise bouts elicit similar blood pressure reductions (^13,27). A question therefore arises as to what could explain these conflicting findings? Cunha et al. (¹⁴) investigated PEH after short-duration cycling (105 ± 29 kcal), walking (113 ± 19 kcal), and running (141 ± 42 kcal) maximal exercise tests. Only running, which was the exercise mode associated with the greatest energy expenditure, elicited a significant reduction in blood pressure compared with a control session. From a practical perspective, the magnitude of PEH seems to be dependent on exercise volume, as reflected by energy expenditure. Notably, among 7 previous studies that directly compared the effects of continuous vs. accumulated exercises on PEH, 5 equated total work from the external work completed (^2,5,22,32,33), whereas 2 studies used isocaloric conditions, and concluded that accumulated exercise elicited similar reductions in blood pressure to continuous exercise (^13,27). How work is equated is an important methodological issue that confounds the interpretation of studies that compared the acute effects of continuous versus accumulated exercise on PEH. The studies that used cycle ergometry (^2,22) did not apply isocaloric bouts, and therefore, susceptible to such confounding. Considering that cycling is frequently used in aerobic training, knowledge about the impact of multiple short bouts of cycling on PEH could have clinically important implications, and further research is warranted.

Changes in autonomic cardiac control, as measured by heart rate variability (HRV) and reflecting beat-to-beat changes in HR and the sympathovagal interaction obtained by the variation of both instantaneous HR and R-R intervals within the cardiac cycle (⁴²), seem to influence blood pressure after exercise (^7,43). It is known that blood pressure is determined by the relationship between cardiac output (Q) and systemic vascular resistance, cardiac (central), or vascular (peripheral) mechanisms that reflect changes in central regulation (⁸), leading to attenuation of the blood pressure response in the postexercise recovery. Evidence about the role of cardiac autonomic control in PEH is controversial, however. Some studies suggest decreased sympathetic activity and increased parasympathetic activity concomitant to PEH (³³), whereas others suggest that a compensatory increase in sympathetic activity would occur to offset the blood pressure reduction and baroreflex resetting (^13,14,39,43), or that no changes would occur (^3,32). The extent to which PEH accompanies a shift in cardiac autonomic balance therefore remains unclear and requires further investigation.

The main aim of this study was to compare the effects of continuous and accumulated bouts of cycling, matched by intensity and energy expenditure, on PEH in prehypertensive men. A second aim was to investigate the relationships between changes in blood pressure vs. changes in sympathovagal balance after each acute exercise bout.

Methods

Experimental Approach to the Problem

Each participant visited the laboratory 5 times. During the first visit, participants were familiarized with the equipment and experimental procedures, then they completed a preparticipation questionnaire for assessment of cardiovascular risk, and then had their blood pressure measured to ensure that they met the study inclusion criteria. On the second visit, anthropometric measurements were taken followed by resting oxygen uptake (V̇o₂), blood pressure, and HRV assessments for 60 minutes (“control” condition). On the third visit, a maximal cardiopulmonary exercise test (CPET) on a cycle ergometer was performed to determine V̇o₂max. Approximately 72 hours after the CPET, 2 isocaloric exercise bouts were performed at 75% of oxygen uptake reserve (V̇o₂R). During one of the visits, the exercise bout was continuous and expended a total of 400 kcal. During the other visit, the exercise bout was accumulated and consisted of 2 × 200-kcal bouts, separated by 1 hour of passive rest, during which blood pressure and HRV were assessed. Allocation of test order for the continuous and accumulated exercise bouts was randomized and counter-balanced across participants. The exercise bouts were separated by 48–72 hours. Before the exercise and control conditions, baseline assessments were performed during 10 minutes of bed rest in a quiet darkened environment with the final 5 minutes used for data collection. Within 5 seconds of exercise (or control session) termination, participants were placed in the supine position, and data collection began 5 minutes after exercise for a period of 60 minutes in a quiet room kept at a relatively constant temperature and relative humidity (ranging from 21 to 23° C and 50–70%, respectively). The participants were instructed not to engage in any physical activity during the 48 hours before and after each laboratory visit. All visits were conducted at approximately the same time of day (between 07:00 and 11:00 am). Exercise bouts were performed on a cycle ergometer (Cateye EC-1600; Cateye, Tokyo, Japan), with the seat height individually set and standardized across all exercise bouts for a given participant.

Subjects

Table 1 shows descriptive statistics for age, anthropometrical variables, resting physiological variables, maximal CPET responses, and HR, absolute V̇o₂, and time to achieve 400 kcal during CONTIN and accumulated (i.e., INTER1 and INTER2) isocaloric exercise bouts of cycling at 75% V̇o₂R. On average, participants were overweight, had prehypertension, and had above-average physical fitness for men of their age (¹).

Ten apparently healthy prehypertensive men, aged 23–34 years, participated in the study. Inclusion criteria consisted of a mean screening SBP of 120–139 mm Hg and DBP of 80–89 mm Hg (²¹). All participants were recreationally active, performing 20–60 minutes of exercise per session on 2–5 days per week, for at least 6 months before the study. The exclusion criteria were: (a) CVD and diabetes; (b) use of drugs that could affect the cardiovascular responses, or any ergogenic substances; (c) smoking; and (d) bone, joint, or muscle problems that could limit the performance of exercise. The study gained approval from the University of Rio de Janeiro State ethics committee (reference 3082/2011) and participants were informed of the benefits and risks associated with the study before providing written informed consent to participate.

Blood pressure screening was performed by a single evaluator using a calibrated mercury-column sphygmomanometer (Heidji; Press Control Indústria e Comércio Ltda, São Paulo, Brazil) and a stethoscope (Sprague Rappaport; Omron, Santa Monica, CA, USA), after participants remained seated for 10 minutes, in accordance with American Heart Association recommendations (³⁴). Participants were instructed to remain relaxed and avoid talking during the measurements. The cuff was placed on the right arm so that the inferior extremity remained at a level within 2.5 cm of the antecubital fossa. The arm was supported at heart level and the bladder of the cuff encircled at least 80% of the arm circumference. The mercury column was deflated at 2–3 mm Hg·s⁻¹ until Korotkoff sounds were heard that corresponded to systolic (first sound) and diastolic (fifth sound) values. The readings were registered to the nearest 2 mm Hg. The blood pressure used for screening participants was calculated as the mean of 3 readings taken at 5-minute intervals.

Procedures

Experimental Blood Pressure Assessment

Resting blood pressure determined before and after each exercise bout and the nonexercise control session was assessed by an oscillometric device (Spacelabs Medical model 90207; Spacelabs, Inc., Redmond, WA, USA). Blood pressure monitoring followed standard procedures (³⁸) using the criteria of the British Hypertension Society (²⁹), including a calibration check before each experiment according to the manufacturer's instructions. Blood pressure recordings after exercise bouts and the nonexercise control session were obtained during 60 minutes at 20-minute intervals in a quiet environment and in a supine position. The control session mimicked the exercise bouts in that participants remained seated at rest for 20 minutes and blood pressure was assessed using the same protocol as that used before and after the exercise bouts in a supine position.

Heart Rate Variability Assessment

The HR and HRV were recorded concomitantly with blood pressure using a telemetric HR monitor (RS800cx; Polar, Kempele, Finland). The R-R intervals were downloaded by Polar Precision Performance Software (Polar) and averaged for each 30-second window using a sampling frequency of 1,000 Hz. Before analysis, all R-R intervals were visually inspected for artifacts to make interpolation corrections on the sequences (⁴²). This was necessary in less than 1% of the sequences for each participant. A fast Fourier transform (Welch's method) with a Hanning window and 50% overlap was used to estimate the power density spectrum of R-R interval variability using a customized routine (MathWorks, Natick, MA, USA). The beat-by-beat R-R interval series were then converted into equally spaced time series with 200-ms intervals using cubic spline interpolation (⁴²).

The ratio between low-frequency and high-frequency bands (LF:HF) was used as an index of sympathovagal balance, with the LF band (0.04–0.15 Hz) being considered as a marker of sympathetic predominance and the HF band (0.15–0.50 Hz) as a marker of parasympathetic predominance (¹⁰). The spectral values were expressed as normalized units (n.u.). To meet the stability requirement for performing spectral analysis, the first 5-minute interval after each exercise bout was omitted from all HRV analyses. The HRV analyses for the control session and following exercise were then used to calculate HRV indices according to previously established guidelines (⁴²).

Resting V̇o₂ Assessment

Resting V̇o₂ was determined before calculation of %V̇o₂R using well-controlled procedures recommended by Compher et al. (⁹). These included abstentions from physical exercise, alcohol, soft drinks, and caffeine in the 24 hours preceding the assessment and fasting at least 8 hours before the assessment. In the laboratory, participants remained awake in a quiet environment for 10 minutes, after which the V̇o₂ was measured for 40 minutes in the supine position. The resting V̇o₂ was recorded as the average of the last 5 minutes of steady-state data assessed during 35–40 minutes (within-subject coefficient of variation ≤10%) (¹²). The resting V̇o₂ was always measured at the same time of the day between 07:00 and 11:00 am

Maximal and Submaximal Exercise Tests

The ramp-incremented maximal CPET was performed as described elsewhere (¹¹). The power output increment was individualized to elicit each participant's limit of tolerance in approximately 10 minutes. The criteria for test termination followed the recommendations of the American College of Sports Medicine (ACSM) (¹). The test was considered to have elicited peak capacity when at least 3 of the following criteria were observed (¹⁸): (a) maximum voluntary exhaustion defined by attaining a 10 on the Borg CR-10 scale; (b) ≥90% predicted maximal HR (220 − age), or presence of an HR plateau (ΔHR between 2 consecutive power outputs ≤4 b·min⁻¹); (c) presence of a V̇o₂ plateau (ΔV̇o₂ between 2 consecutive power outputs <2.1 ml·kg⁻¹·min⁻¹); and (d) respiratory exchange ratio >1.10.

Based on the V̇o₂max achieved during the CPET and the resting V̇o₂, values corresponding to 75% V̇o₂R were calculated to determine the intensity of the 2 isocaloric exercise bouts. The absolute V̇o₂ values obtained from the %V̇o₂R equation were used to calculate the associated cycling power outputs (mean ± SD, 257 ± 55 W) by applying the ACSM metabolic equation (¹). Each exercise bout was preceded by a 5-minute warm-up at 30 W and 65–75 rev·min⁻¹. Expired gases were collected during exercise bouts using the metabolic cart. The exercise bouts were terminated when each participant had achieved a total energy expenditure of 400 or 200 kcal in continuous or accumulated acute exercise bouts, respectively, and followed by 60 minutes of recovery in the supine position to measure blood pressure and HRV.

Pulmonary gas exchanges were determined using breath-by-breath analyses with a VO2000 metabolic cart (Medical Graphics, Saint Louis, MO, USA). Gas exchange data were calculated, averaged, and recorded every 30 seconds, which provided a good compromise between removing noise in the data while maintaining underlying physiological trends (²⁴). Before testing, gas analyzers were calibrated according to the manufacturer's instructions, using a certified standard mixture of oxygen (17.01%) and carbon dioxide (5.00%), balanced with nitrogen (AGA, Rio de Janeiro, RJ, Brazil). Flows and volumes of the pneumotachograph were calibrated with a syringe graduated for 3 L capacity (Hans Rudolph, Kansas, MO, USA).

Statistical Analyses

All statistical analyses were performed using IBM SPSS Statistics 22 software (SPSS, Inc., Chicago, IL, USA). Descriptive statistics are presented as mean ± SD. The effect of condition (control, continuous exercise [CONTIN], first intermittent exercise bout [INTER1], and second intermittent exercise bout [INTER2]) and time (baseline and 60-minute postexercise period [time-averaged at 20, 40, and 60 minutes]) on blood pressure and HRV indices were analyzed using marginal models using the SPSS MIXED procedure. The best fitting covariance structure was identified as that which minimized the Hurvich and Tsai's criterion value. Where there was a statistically significant main effect for condition or a significant condition × time interaction effect, post hoc pairwise comparisons with Sidak-adjusted p values were obtained. Pearson correlations were used to determine the relationships between changes in SBP and DBP vs. changes in the LF:HF ratio for the 60 minutes after the exercise bouts. Two-tailed statistical significance was accepted as p ≤ 0.05.

Results

Table 1.: Baseline participant characteristics (N = 10).

Acute Blood Pressure Responses to Cycling Bouts

Figure 1 shows the average blood pressure responses during 60 minutes after the control session and each exercise bout. There were main effects for condition (SBP: F = 28.9, p < 0.001; DBP: F = 10.9, p < 0.001; and MAP: F = 27.8, p < 0.001) and time (SBP: F = 229.2, p < 0.001; DBP: F = 7.9, p = 0.009; and MAP: F = 110.3, p < 0.001). A significant condition × time interaction showed that the differences between control and the exercise conditions decreased over time for SBP (F = 4.1, p < 0.001), DBP (F = 4.0, p = 0.001), and MAP (F = 3.9, p = 0.001). For example, the largest reductions in blood pressure after exercise occurred during the first 20 minutes, with significant differences of 3.9–6.2, 2.8–3.6, and 3.5–4.4 mm Hg observed between control and the postexercise periods for SBP, DBP, and MAP, respectively. Compared with control, on average, CONTIN, INTER1, and INTER2 elicited reductions in SBP of 3.4 ± 2.5 mm Hg (95% CI = 1.7–5.1 mm Hg, p < 0.001), 2.2 ± 2.4 mm Hg (95% CI = 0.6–4.0 mm Hg, p < 0.001), and 4.4 ± 2.5 mm Hg (95% CI = 2.5–6.0 mm Hg, p < 0.001), respectively. No significant differences in SBP were observed between CONTIN and INTER2 (mean difference = 0.9 mm Hg, 95% CI = −0.9 to 2.6 mm Hg, p = 0.934), or between CONTIN and INTER1 (mean difference = −1.1 mm Hg, 95% CI = −2.8 to 0.6 mm Hg, p = 0.652); however, SBP was significantly lower after INTER2 than INTER1 (mean difference = 2.0 mm Hg, 95% CI = 0.2–3.7 mm Hg, p = 0.015). Unlike SBP, on average, there was no significant difference in DBP reduction after CONTIN ([p = 0.320); except the mean difference of −2.8 mm Hg between control and CONTIN at 20 minutes [p ≤ 0.05]) and INTER1 compared with control (p = 0.985), whereas a significant difference was observed between INTER2 vs. control (mean difference = −2.7 mm Hg, 95% CI = −0.3 to 5.2 mm Hg, p = 0.045). There was no significant difference between DBP responses among the exercise conditions (p = 0.771–0.999). Mean arterial pressure was 2.5 ± 2.1 and 3.3 ± 2.1 mm Hg lower after CONTIN (95% CI = 0.7–4.3, p = 0.001) and INTER2 (95% CI = 1.6–5.1, p < 0.001) compared with control, respectively, whereas there was a nonsignificant difference between INTER1 vs. control (p = 0.177) (except the mean difference of −2.2 mm Hg between control and INTER1 at 20 minutes [p ≤ 0.05]). Comparing the exercise conditions, there was no significant difference between CONTIN vs. INTER1 (p = 0.832) or CONTIN vs. INTER2 (p = 0.968), except a significant reduction after INTER2 compared with INTER1 (MAP: mean difference = 1.8 mm Hg, 95% CI = 0.3–3.6 mm Hg, p = 0.043).

Figure 1.: Mean ± SD change in SBP, DBP, and MAP (mean value for condition minus mean value for control) at baseline and postexercise recovery periods. *Significantly lower than control (p ≤0.05 to <0.001). †Significantly lower than INTER1 (p ≤ 0.05). CONTIN = continuous cycling bout; INTER1 = first intermittent cycling bout; INTER2 = second intermittent cycling bout; SBP = systolic blood pressure; DBP = diastolic blood pressure; and MAP = mean arterial pressure.

Acute Cardiac Autonomic Responses to Cycling Bouts

Figure 2 shows the average cardiac autonomic responses at baseline and during 60 minutes after the control session and each exercise bout. There were significant main effects for condition (HR: F = 10.9, p < 0.001; LF: F = 46.4, p < 0.001; HF: F = 50.6, p < 0.001; and LF:HF ratio: F = 23.1, p < 0.001), time (HR: F = 7.9, p = 0.009; LF: F = 4.0, p = 0.010; HF: F = 5.1, p = 0.008; and LF:HF ratio: F = 4.4, p < 0.022), and a significant condition × time interaction only for HR (F = 4.0, p = 0.001). On average, HR was 12.8 ± 2.9 b·min⁻¹ (95% confidence interval [CI] = 4.4–21.1 b·min⁻¹, p < 0.001), 11.5 ± 4.2 b·min⁻¹ (95% CI = 3.2–19.8 b·min⁻¹, p = 0.001), and 10.9 ± 4.1 b·min⁻¹ (95% CI = 2.6–19.2 b·min⁻¹, p = 0.002) higher after CONTIN, INTER1, and INTER2 compared with control, respectively. Findings from time-frequency spectral analysis of HRV, for example, showed that CONTIN elicited a 25.3 ± 8.0-unit increase in LF compared with control (95% CI = 18.1–32.5 units, p < 0.001), whereas INTER1 and INTER2 elicited increases of 23.9 ± 8.9 units (95% CI = 17.1–30.7 units, p < 0.001) and 26.6 ± 3.5 units (95% CI = 19.8–32.8 units, p < 0.001), respectively. Unlike LF, HF was 26.2 ± 9.6 units (95% CI = 18.4–34.0 units, p < 0.001), 23.4 ± 11.0 units (95% CI = 16.2–30.5 units, p < 0.001), and 26.2 ± 5.9 units (95% CI = 20.1–32.3 units, p < 0.001) lower after CONTIN, INTER1 and INTER2 compared with control, respectively. Like HR and LF, the LF:HF ratio was significantly higher after CONTIN (p < 0.001), INTER1 (p < 0.001) and INTER2 (p < 0.001) compared with control. However, in all HRV indices, no significant differences were observed among exercise conditions (p > 0.05).

Figure 2.: Mean ± SD change in HR, LF, HF, and LF:HF ratio (mean value for condition minus mean value for control) at baseline and postexercise recovery periods. *Significantly lower than control (p ≤0.05 to <0.001). CONTIN = continuous cycling bout; INTER1 = first intermittent cycling bout; INTER2 = second intermittent cycling bout; HR = heart rate; LF = low-frequency band; HF = high-frequency band; and LF:HF ratio = sympathovagal balance.

Relationships Between Changes in Blood Pressure and Changes in Low-Frequency Band: High-Frequency Band Ratio

Figure 3 shows the relationships between ΔSBP and ΔDBP vs. ΔLF:HF ratio during the 60-minute recovery period after exercise compared with control. Both ΔSBP and ΔDBP were negatively correlated with the ΔLF:HF ratio after CONTIN and INTER2, with Pearson correlation coefficients (r) ranging from −0.64 to −0.65 (p = 0.045–0.041, respectively) for SBP, and −0.26 to −0.71 (p = 0.467–0.021, respectively) for DBP. Only the relationships between ΔSBP and ΔDBP vs. ΔLF:HF ratio after INTER1 or between ΔDBP vs. ΔLF:HF ratio after CONTIN were not significant (p > 0.05).

Figure 3.: Relationships between average changes in blood pressure and the LF:HF ratio during the 60-minute assessment after control and recovery period from CONTIN, INTER1, and INTER2. CONTIN = continuous cycling bout; INTER1 = first intermittent cycling bout; INTER2 = second intermittent cycling bout; SBP = systolic blood pressure; DBP = diastolic blood pressure; and LF:HF ratio = sympathovagal balance.

Discussion

To the best of our knowledge, this study is the first to investigate the extent to which the magnitude of PEH is affected by cycling bouts performed continuously and cumulatively under isocaloric conditions (i.e., same energy expenditure) in prehypertensive men. Three important observations can be derived from the main findings of this study with respect to optimizing exercise prescription for maximizing the magnitude of PEH: (a) There was a significant positive accumulative effect on PEH from accumulated exercise. Splitting the cycling exercise into 2 bouts of short-term exercise (i.e., 2 × 200 kcal) was shown to empower subacute effects on PEH, promoting similar decreases in blood pressure compared with a continuous cycling bout with an equivalent total energy expenditure of 400 kcal. Consequently, exercise prescription with either accumulated or continuous isocaloric exercise can be adopted; (b) these findings also suggest that the exercise volume determines the pattern of the hypotensive response to aerobic exercise, where INTER1 with the same relative intensity (i.e., 75% V̇o₂R) but lower volume (i.e., 200 kcal) promoted lower PEH than INTER2 with a greater exercise volume (i.e., 400 kcal); (c) last, sympathetic (LF component of HRV) and parasympathetic (HF component of HRV) activities remained significantly increased and decreased during the 60-minute exercise recovery, resulting in a sympathetic overload (expressed by the LF:HF ratio) that was inversely correlated with the magnitude of PEH, regardless of CONTIN or INTER2 acute exercise. This finding indicates that the recovery pattern of cardiac autonomic activity may have an important role in eliciting PEH.

To date, findings from most previous studies support the idea that accumulated exercise bouts elicit a greater PEH than continuous exercise bouts using treadmill (^5,32,33) and cycle ergometry (^2,22). Park et al. (³³), for example, compared blood pressure responses after continuous (40 minutes) and accumulated (4 × 10 minutes with rest intervals of 50 minutes) bouts of treadmill walking, at an intensity of 50% V̇o₂peak, in 21 prehypertensive adults (SBP and DBP = 131.9 ± 1.1 and 82.5 ± 1.4 mm Hg, respectively and V̇o₂max = 34.5 ± 1.6 ml·kg⁻¹·min⁻¹). The continuous exercise bout resulted in lowered SBP and DBP for 7 hours into recovery, whereas the accumulated bout provided greater PEH, with SBP and DBP significantly reduced for 11 and 10 hours postexercise, respectively. However, this study disagrees with this view because the magnitude of PEH in relation to control was similar in both the CONTIN and INTER2 for cycling (ΔSBP_60-min = −3.4 and −4.3 mm Hg, respectively and ΔDBP_60-min = −2.0 and −2.6 mm Hg, respectively). On the other hand, similar to our findings, Cunha et al. (¹³) observed that accumulated (2 × 200 kcal with rest interval of 60 minutes) and continuous (400 kcal) treadmill running at 75% V̇o₂R elicited similar SBP and DBP reductions compared with a control session (∆SBP = −6 and −7 mm Hg, respectively and ∆DBP = −5 and −6 mm Hg, respectively) among 10 hypertensive men. Beyond that, the authors provided further analysis showing that continuous and second accumulated bouts matched for total energy expenditure of 400 kcal induced greater blood pressure reduction compared with the first accumulated bout performed with equivalent intensity (i.e., 75% V̇o₂R) but a lower energy expenditure (200 kcal) (i.e., ∆SBP = 2.1 and 4.3 mm Hg, respectively and DBP = 3.7 and 4.8 mm Hg, respectively). In other words, it is feasible to think that the exercise volume involved, which seems to be a major determinant of PEH, is likely to be one of the main reasons why the results of this study differ from previous research reporting different blood pressure responses after continuous and accumulated acute aerobic bouts because all these studies failed to match the exercise volume by energy expenditure.

It is clear that accumulated exercise bouts can be a useful tool for prescribing aerobic exercise in different populations because its acute effect on the magnitude of the PEH seems to be similar or equal to continuous exercise. In addition, other advantages may make prescribing accumulated exercise more favorable, such as a better strategy to improve exercise adherence (²⁰), because this strategy seems to be more palatable and easier to maintain (²⁸). Sedentary individuals have low tolerance to prolonged efforts, such as continuous exercise lasting 30–60 minutes, and accumulated bouts also could minimize this issue. Accumulated bouts could even allow for higher intensity exercise, which chronically may result in greater benefits than continuous exercise with moderate intensity and long duration in improving cardiorespiratory fitness, body composition, total cholesterol, low-density lipoprotein cholesterol, serum triglycerides, insulin sensitivity, and glucose control (⁴¹). All these favorable changes in health status from engaging in vigorous-intensity exercise (i.e., 60–85% V̇o₂R) have been identified as independent risk factors for hypertension (^19,40).

Regarding postexercise cardiac autonomic control, our findings agree with previous reports (^13,14,39,43), because the HRV spectral analysis indicated that during recovery from continuous and accumulated cycling bouts, sympathetic activity (LF band) increased, whereas parasympathetic activity (HF band) decreased, resulting in higher sympathovagal balance (LF:HF ratio) concomitant with a reduction in blood pressure (Figures 1 and 2). Moreover, the acute reductions in blood pressure after CONTIN and INTER2 were negatively correlated with changes in sympathovagal balance, meaning that the greater the magnitude of PEH, the greater the increase in relative sympathetic activity (Figure 3). Nonetheless, the reason for this inverse relationship between changes in blood pressure and changes in the LF:HF ratio during exercise recovery remains unclear. Some studies have shown, for example, that the operating point of the arterial baroreflex seems to be at low values of blood pressure (^7,25), indicating that the elevated sympathetic activity and reduced vagal activity of HR may be associated with the hypotensive effect of exercise that reduces the discharge of pressoreceptors, causing less inhibition of sympathetic activation and lower parasympathetic activation–mediated reflex arc dependent on arterial baroreceptors. This is a physiological response to offset the reduction in blood pressure and compensate for resetting of the baroreflex (¹⁷). If this is indeed the case, it is plausible that the hypotensive effect would somehow rely on the ability of peripheral vasodilation mechanisms to overcome such increases in sympathetical activity.

On the other hand, the absence of a correlation between blood pressure and sympathovagal balance in this study occurred only after INTER1 (Figure 3). Within a practical perspective, whether or not a correlation between blood pressure and sympathovagal balance is observed after exercise might be a result of exercise volume—in other words, the compensatory response related to acute blood pressure lowering and shift in cardiac autonomic balance might also be associated with exercise volume. It has been advocated that exacerbated hemodynamic responses after exercise may be influenced by the amount of muscle work, which would increase the exercise pressor reflex (ergoreflex) through afferent stimuli from muscle ergoreceptors (mechanoreceptors and metaboreceptors) (^8,16,26). The increased muscle afferent signaling would contribute to a higher sympathetic activity during exercise and to a consequent “resetting” of the arterial baroreflex during the postexercise period, reducing sympathetic outflow and lowering blood pressure (^15,16). It is, therefore, plausible that at least to some extent, the magnitude of blood pressure reduction and the shift of sympathovagal balance after an aerobic exercise bout might rely on the amount of overall volume, as expressed by the energy expenditure. This could partially explain the total absence of correlation between blood pressure and sympathovagal balance only after INTER1 (i.e., the exercise bout with the lowest energy expenditure). Further research is certainly warranted to clarify these issues.

Another issue to be addressed is the effect of the recovery period between accumulated intermittent bouts on the acute blood pressure and cardiac autonomic control responses. Although there is no consensus in the literature on this issue, it is worth noting that previous studies have adopted 3–4 sets of 10 minutes of exercise interspaced by 10 minutes (²²), 50 minutes (^32,33), or 4 hours (^2,5) of rest periods. From a practical perspective, it is feasible to think that this wide range observed for the recovery period between intermittent bouts (i.e., 10 minutes–4 hours) could directly affect the phenomenon of PEH because the immediate postexercise hyperemia—one of the mechanisms underlying hypotension—can last from several seconds up to 20 minutes (^4,16). Additional research is, therefore, needed to verify any changes in PEH in response to different recovery periods accumulated between intermittent bouts.

Practical Applications

The PEH was favorably affected by the accumulation of cycling bouts. In practical terms, splitting the volume of exercise into 2 bouts of shorter-term exercise, with the same total energy expenditure, was as effective as the more traditional approach of using continuous exercise to promote the postexercise hypotensive effects of aerobic exercise. In addition, exercise volume measured by energy expenditure markedly influences the PEH response, regardless of whether the exercise is performed continuously or cumulatively. In this context, aerobic exercise that involves a higher volume elicits greater PEH than that involving a smaller volume. Furthermore, the magnitude of PEH was associated with vagal inhibition and prolonged elevation in sympathetic activity during recovery from aerobic exercise involving greater volume in prehypertensive men. These findings may have important implications for prescribing aerobic exercise as a long-term intervention for lowering blood pressure.