Journal of Exercise Physiologyonline

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1 Journal of Exercise Physiologyonline 36 October 2017 Volume 20 Number 5 Editor-in-Chief Official Research Journal of Tommy the American Boone, PhD, Society MBA of Review Exercise Board Physiologists Todd Astorino, PhD Julien Baker, ISSN PhD Steve Brock, PhD Lance Dalleck, PhD Eric Goulet, PhD Robert Gotshall, PhD Alexander Hutchison, PhD M. Knight-Maloney, PhD Len Kravitz, PhD James Laskin, PhD Yit Aun Lim, PhD Lonnie Lowery, PhD Derek Marks, PhD Cristine Mermier, PhD Robert Robergs, PhD Chantal Vella, PhD Dale Wagner, PhD Frank Wyatt, PhD Ben Zhou, PhD Official Research Journal of the American Society of Exercise Physiologists ISSN JEPonline Strength Training Methods Does Not Affect Post- Exercise Hypotension and Heart Rate Variability Daniel Rodriguez 1,2, Koichi Nakazato 2, Steven Fleck 3, Luciano F. Pontes Jr. 4, Mario A. Charro 5, Gustavo Alegretti 1, Danilo S. Bocallini 1, Aylton Figueira Jr. 1 1 Faculty of Physical Education - University São Judas Tadeu. São Paulo / SP Brazil, 2 Nippon Sports Science University, Setagaya-ku, Tokyo Japan, 3 Department of Kinesiology, University of Wisconsin, Eau Claire / WI United States of America, 4 School of Arts, Sciences and Humanities, University of São Paulo, São Paulo / SP Brazil, 5 Faculty of Physical Education Centro Universitário das Faculdades Metropolitanas Unidas, São Paulo / SP Brazil-, 1 Faculty of Physical Education - University São Judas Tadeu, São Paulo / SP Brazil, 1 Faculty of Physical Education - University São Judas Tadeu, Paulo / SP Brazil ABSTRACT Rodriguez D,Nakazato K, Fleck S, Pontes LF, Charro MA, Bocallini DS, Figueira A. Strength Training Methods Does Not Affect Post-Exercise Hypotension and Heart Rate Variability. JEPonline 2017;20(5): The purpose of this study was to determine the influence of resistance exercise (RE) training methods (circuit [C], multiple sets [MS]) on postexercise hypotension (PEH) and heart rate variability (HRV) of untrained normotensive adults. The subjects (N = 25; 46.5 ± 4.9 yrs; mean arterial pressure [MAP] 96.4 ± 4.0 mmhg; resting heart rate [HR] 66.5 ± 4.7 beats min -1 ) performed C and MS sessions (12 exercises 3 sets; 14 to 17 reps; 60% of 1RM) with equal total work load. Their blood pressure (BP) and HRV were monitored 20 min before and 90 min after the RE sessions. Autonomic regulation was evaluated by normalized low-frequency (LFnu) and high-frequency (HFnu) components of HRV. The MAP remained significantly reduced throughout the post-exercise period compared to rest for both RE sessions (C = -6.1 ± 1.3 mmhg and MS = -6.3 ± 1.5 mmhg; P<0.05), but was not significantly different between C

2 and MS. The LFnu increased while the HFnu decreased following both RE sessions (P<0.05). Thus, both methods caused a similar PEH response. The HFnu increase suggests that PEH is accompanied by increased sympathetic modulation of the heart, which has been previously described for the MS but not for C. This study indicates that PEH is not affected by exercise method, and is determined by central nervous system changes. The cardiovascular response is likely associated with other mechanisms, such as plasma blood volume. Keywords: Heart Rate Variability; Post-Exercise Hypotension; Resistance Exercise 37 INTRODUCTION Regular resistance exercise (RE) is an important strategy to control systemic blood pressure (BP), both in normotensive and hypertensive adults (1,2). One single session of RE has been shown to induce post-exercise hypotension (PEH), due to physiological responses that may temporarily influence and/or reduce BP (4,8,9,30). The popularity of RE training is increasing in different population segments due to the evidence that shows health-related-benefits, including cardiovascular health benefits. Both the American College of Sports Medicine (1) and the American Heart Association (2) recommend that RE in association with an aerobicbased exercise program as an efficient strategy to prevent, treat, and control hypertension. However, available data on RE training and PEH remains scarce and controversial. Various studies have demonstrated an increase in BP (14), no significant change in BP (14), and a significant decrease in BP (20,30,31,33) following RE. Thus, several physiological hypotheses have been postulated to explain PEH. The overall physiological response is a decrease in post-exercise BP and, it seems that the sympathetic regulation of heart rate is elevated while the parasympathetic regulation remains unchanged after RE (22,23). Simultaneously, the endothelium vasodilator agents such as nitric oxide, prostaglandins, adenosine, and potassium release (13) induce the lowering of peripheral vascular resistance. Following aerobic exercise, a hypotensive response may occur in a dose-response pattern in relation to the volume and intensity of the exercise performed (8,9, 15,16,22). Nevertheless, the RE presents a more complex interrelationship between training volume and intensity, leading to confusing results concerning the PEH response (31). While many RE studies (20,30,31,33) demonstrate a PEH response, the data concerning the effect of different types of RE training methods on the PEH response is lacking. For example, the two most popular RE-based training programs prescribed in health and fitness centers to the general population are circuit training (C) and traditional multiple-set training (MS). Yet, the effect of C and MS programs on cardiovascular responses has not been previously reported. The purpose of this study was to investigate the effect of these two types of RE training (C and MS) on the post-exercise autonomic and hypotensive response in healthy adult males. METHODS Subjects Twenty-five normotensive and clinically healthy male adults between 40 and 50 yrs old (46.50 ± 4.98 yrs) were recruited. None of the subjects had participated in a strength-training

3 program for at least six months before the study were recruited. None of the subjects was undergoing treatment for infectious illnesses or using medication that could alter their cardiovascular, immunological, hormonal, or metabolic response at rest or during exercise. Individuals who followed a restrictive diet to reduce weight or taking nutritional supplements and/or anabolic steroids were excluded. The procedures for this study were approved by the São Judas Tadeu University Human Research Review Committee (São Paulo/Brazil), and all subjects provided an informed written consent before participation. Measurements Before each testing session, the subjects remained in a seated position for 20 min (preintervention period) before the resting BP measurement was determined. After each RE training session, the subjects returned to the laboratory where they rested for 90 min (postintervention period) in the seated position. The air temperature was kept between 20 and 22 C. The subjects BP was measured in pre-intervention and seven times post-intervention, at 0, 15, 30, 45, 60, 75, and 90 min. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured in the left arm by an oscillometric blood pressure monitor (BP A13, Microlife, USA). Mean blood pressure (MBP) was calculated as the sum of DBP plus one-third of pulse pressure. The protocol for the blood pressure measurement followed the recommendations of the American Heart Association (2). Heart rate and RR intervals were recorded by telemetry using a frequency meter RS 800 (Polar Electro Oy, Finland). The RR intervals were collected for autonomic assessment at 10 min pre-intervention and at 0, 30, 60, and 90 min post-intervention. After collection with a sampling frequency of 1,000 Hz, an RR interval difference exceeding 20% of the previous interval was filtered off automatically using Polar Precision Performance software (Kempele, Finland. version ). Then, the records of the RR intervals were edited manually by visual inspection in an attempt to avoid artifacts that might contaminate the analysis. The autonomic response data were analyzed for heart rate variability (HRV) using spectral analysis of auto-regressive RR interval variability. The components of HRV corresponding to autonomic activity were determined according to procedures described by the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electromyography (12). The values of the integration of successive modules spectral bands from Hz to 1 Hz were used to calculate the spectral variability of the entire spectrum (total power). The integration of values between successive heart rate ranges was divided as follows in relation to the frequency domain: (a) very low-frequency component (VLF, Hz to 0.04 Hz); (b) low-frequency component (LF, 0.04 Hz to 0.15 Hz); and (c) high-frequency component (HF, 0.15 Hz to 0.4 Hz). The cardiac sympathovagal index was calculated as the ratio between LF and HF (LF/HF ratio). The HF and LF components were reported in normalized units (nu), which represent the relative value of each power component in proportion to the total power minus the very low-frequency component (VLF Hz) (12). The components LF and HF were then converted to normalized units (nu), which represent the relative value of each power component in proportion to the total power minus very low- 38

4 frequency component (VLF Hz) using the equations: LFnu = HF / (Total Power VLF) 100 and HFnu = F / (Total Power VLF) 100. The normalized values of RR interval variability were considered markers of sympathetic nervous system and parasympathetic nervous system activity, respectively. The normalized ratio of the components and LFnu, HFnu (LF/HF) was considered as an indicator of sympathovagal balance (30). Prior to testing, all subjects underwent a familiarization period of two weekly sessions (3 sets of 20 reps for each exercise with the minimal load permitted by the equipment) on nonconsecutive days over a 4-wk period. The determination of the intensity to be used for both training systems was set through the one maximal repetition (1RM) test for all sessions (Table 1). The 1RM was determined one week before the beginning of the experimental procedures according to the protocol described before (21). The starting position, exercise movement, and range of motion were standardized as commonly described for each exercise. A maximum of 5 attempts to determine the 1RM was allowed for each exercise. If this number was exceeded, the test was repeated on another day with at least a 72-hr interval between tests. Experimental Procedures The subjects were instructed to: (a) avoid physical exercise and alcohol intake during the 48 hrs before the experimental procedures; (b) avoid smoking, consuming caffeine, or taking medications for 12 hrs before the experimental procedures; (c) have a light meal 2 hrs before the experimental procedures; and (d) stay hydrated by consuming 0.5 liters of water on the night before and in the morning of each experimental trial. Each subject was unaware of what sessions he was going to perform until the exercise session began. All subjects performed both the C and MS sessions between 1 and 3 pm, in random order with a minimum interval of 7 days between sessions (8). The RE sessions followed the recommendations of the American College of Sports Medicine (1) for beginners. The two RE sessions consisted of 12 strength exercises (lat pulldown, trunk crunch, leg press, barbell bench press, seated leg curl, back hyperextension, seated row, seated hip adduction, shoulder press, leg extension, and side oblique crunch). All sets in both exercise sessions consisted of between 14 and 17 reps at 60% 1RM. The performance of the C session was configured so that each subject could perform all exercises in a circuit manner (i.e., accomplishing 1 set of an exercise and, then progressing to the next one). The average interval between successive exercises in the circuit session was 10 sec. The MS session consisted of performing all 3 sets of an exercise before progressing to the next one. The rest period between exercises and sets was 1 min. The MS was composed of the same exercises in the same order and the same load and number of repetitions as the C session. Statistical Analysis The data are presented as mean ± SD. Changes in all variables in each experimental session were calculated as the difference in values measured in the pre-intervention and the postintervention periods. A two-way ANOVA for repeated measures (SPSS Version 13.0, USA) was used to compare the MS and C sessions and the measurements before and 15, 30, 45, 60, 75, and 90 min after the exercise programs. Data distribution was verified by the Shapiro Wilk test, and a natural logarithmic (ln) transformation was used when necessary (for HFnu 39

5 and LF/HF). Post-hoc comparisons were assessed by the Newman Keuls test, and P<0.05 was the threshold for statistical significance. RESULTS The subjects characteristics are presented in Table 1. Measures of cardiovascular variables at rest are shown in Table 2. The values were within the normal limits of systolic blood pressure as well as other functional indicators. Table 1. Subjects Age and Anthropometric Characteristics. 40 Variable (N = 15) Mean ±SD Age (yrs) Mass (kg) Height (cm) BMI (kg m -2 ) Fat (%) ±SD = Standard Deviation Table 2. Cardiovascular Characteristics at Rest. Variable (N = 15) Mean ±SD HR at Rest (beats min -1 ) RPP at Rest (beats min -1 mmhg) SBP at Rest (mmhg) DBP at Rest (mmhg) MAP at Rest (mmhg) RR (ms) HFnu LFnu HF/LF SD = Standard Deviation; HR = Heart Rate; beats min -1 = Beats Per Minute; RPP = Rate Pressure Product; SBP = Systolic Blood Pressure; DBP = Diastolic Blood Pressure; MAP = Mean Arterial Pressure; RR = RR Wave Interval; HF = High Frequency; LF = Low Frequency; nu = Normalized Unit

6 Values of muscle strength determined by 1RM tests are presented in Table 3. The absolute value is 100% of 1RM and the relative loads are 60% of 1RM. Table 3. Maximum Workload of Male adults on the 1RM Test and 60% Training Load. Exercises 100% (1RM) 60% of 1RM 41 (kg ± SD) (kg ± SD) Lat Pulldown 85.6 ± ± 7.7 Leg Press ± ± 9.6 Barbell Bench Press 70.2 ± ± 6.7 Seated Leg Curl ± ± 8.2 Seated Row 82.9 ± ± 7.0 Seated Hip Abduction 98.5 ± ± 7.8 Shoulder Press 51.4 ± ± 6.9 Leg Extension 96.4 ± ± 8.4 SD = Standard Deviation The RR interval values were significantly reduced at all times relative to the pre-exercise in both the C and MS sessions. There was no significant difference at any time point in the RR interval between the C and MS sessions (Table 4). The other parameters (LF, HF, LF/HF) related to HRV were also significantly reduced compared to pre-exercise. Although the postexercise values of HF, LF, and HF/LF ratio were lower at all time points after the MS session compared to the C, no significant differences were observed between the sessions. Table 4. Changes in Autonomic Activity Indices Before and After Circuit (C) or Multiple Sets (MS) Sessions.. Pre-Exercise Post-Exercise 0-15 min min min min RR Interval (ms) C ± ± 0.025* ± 0.028* ± 0.022* ± 0.029* MS ± ± 0.032* ± 0.034* ± 0.037* ± 0.028* LFn u C 65.6 ± ± 3.5* ± 4.3* ± 3.5* ± 3.9* MS 64.1 ± ± 2.3* ± 2.8* ± 3.2* ± 2.6* HFn u C 34.8 ± ± 0.34* ± 0.22* ± 0.21* ± 0.15* MS 36.1 ± ± 0.27* ± 0.21* ± 0.18* ± 0.17* Ratio LF/HF C ± 0.33* ± 0.24* ± 0.22* ± 0.18* MS ± 0.28* ± 0.23* ± 0.19* ± 0.16* R-R, LFn u = Normalized Low Frequency Component of R-R Variability, and HFn u = Normalized High Frequency Component of the R-R Variability, *Significant Difference Compared to Pre-Exercise (P<0.05)

7 Comparison of the pre-exercise and post-exercise measurements showed a significant decrease in SBP after both training sessions (Figure 1). The C session resulted in a significant increase in SBP (P<0.05) immediately after the end of the exercise session compared to pre-exercise session. The increase in SBP at 0 min post-exercise in the C session was significantly higher than the SBP in the MS session at the same time point ( SBP = 28.58%). Fifteen minutes post-exercise SBP of the C session returned to preexercise ( mmhg). Nonetheless, there was a significant difference in relation to the MS session s SBP values ( SBP = 8.81%). At 45 min post-exercise, SBP of the MS session was lower than C session. However, the difference was not significant, and the maximum difference between methods at 60 min after exercise was 3.49%. At all time points post-exercise, except at 0 min post-exercise, the MS session showed a significant reduction in SBP compared to pre-exercise. The C session post-exercise SBP showed a significant decrease at most time points, except at 0 and 60 min post-exercise, when compared to pre-exercise. 42 MS Figure 1. Systolic blood pressure (SBP) after the circuit (C) and multiple sets (MS) methods. Values were Figure 1. Systolic Blood Pressure (SBP) after the Circuit (C) and Multiple Sets (MS) Methods. obtained at rest and for 90 minutes after the exercise protocol, at 15-minute intervals. Mean values are Values shown. *Significant were Obtained difference at Rest compared and for to 90 rest, min p<0.05. After a the Significant Exercise difference Protocol compared at 15-min to Intervals. the MS method, Mean values p<0.05. are shown. *Significant difference compared to rest, P<0.05. a Significant difference compared to the MS method, P<0.05. Both exercise sessions demonstrated a significant reduction in DBP from 0 to 30 min postexercise (Figure 2). The MS session-exercise caused a significant reduction in DBP compared to pre-exercise except at 45 and 60 min post-exercise. The post-exercise DBP for the C session was significantly reduced compared to pre-exercise except at 90 min post-exercise. The differences between the post-exercise DBP of the two sessions were small, ranging from 2.4% (15 min) to 0.22% (30 min), and not statistically significant.

8 MS SM C DBP (mmhg) % -0.22% +0.77% -0.43% -1.29% -1.16% +0.95% % POST INTERVENTION Figure Diastolic blood Blood pressure Pressure (DBP) (DBP) after the after circuit the (C) Circuit and multiple (C) and sets Multiple (MS) methods. Sets (MS) Values Methods. were obtained at rest and for 90 minutes after the exercise protocol, at 15-minute intervals. Mean values are Values were Obtained at Rest and for 90 min After the Exercise Protocol at 15-min Intervals. Mean shown. *Significant difference compared to rest, p<0.05. values are shown. *Significant difference compared to rest, P<0.05. a Significant difference compared to the MS method, P<0.05. The MBP was significantly lower in relation to pre-exercise for all measurements, except at 0 min post-exercise of the C session (Figure 3). No significant differences were observed between the 2 sessions. The maximum difference in MBP shown between the 2 sessions was 3.45% at 0 min post-exercise. MBP (mmhg) ,06 +3,45 +2,52 * * * +1,21-0,20-2,59-2,45 MS SM C -1, POST INTERVENTION Figure Figure Medium Medium blood Blood pressure Pressure (MBP) (MBP) after after the the circuit Circuit (C) (C) and and multiple Multiple sets Sets (MS) (MS) methods. Methods. Values Values were obtained were Obtained at rest at and Rest for and 90 for minutes 90 min after After exercise, the Exercise at 15-minute Protocol at intervals. 15-min Intervals. Mean values Mean are values shown. are *Significant shown. *Significant difference difference compared compared to rest, p<0.05. to rest, P<0.05. a Significant difference compared to the MS method, P<0.05.

9 The post-exercise HR of both sessions was significantly higher than pre-exercise for all measurements (Figure 4). Post-exercise HR of the C session at 0 min post-exercise was significantly greater than that of the MS session at the same time point (P<0.05). Postexercise HR of C was lower, by 4.39% to 6.48, than the MS session at all time points between 15 and 90 min and was significantly lower at 75 and 90 min post-exercise (P<0.05) % * MS SM C HR (bpm) ,11% -6.48% -4.39% -5.48% * a a -4.89% -8.87% % Figure 4. Heart Rate (HR) after the Circuit (C) and Multiple Sets (MS) Methods. Values were Obtained at Rest and for 90 min After the Exercise Protocol at 15-min Intervals. Mean values are shown. *Significant Figure 4. Heart rate (HR) after the circuit (C) and multiple sets (MS) methods. Values were obtained at rest and for 90 minutes after exercise, at 15-minute intervals. Mean values are presented. *Significant difference compared to rest, p<0.05. a Significant difference compared to the MS method, p<0.05. difference compared to rest, P<0.05. a Significant difference compared to the MS method, P<0.05. At 0 min post-exercise the rate pressure product (RPP) of the C session was significantly higher than pre-exercise and compared to the MS session (Figure 5), with a change of 43.15% between pre-exercise and 0 min for the C session (P<0.05). At 0 min and 15 min post-exercise, the C and MS sessions showed very similar RPP values. While from 30 to 90 min post-exercise, the MS showed slightly higher RPP values compared to the C session % SM MS C DP (mmhg/bpm) RPP % % -2.24% -5.01% -8.21% % % POST INTERVENTION Figure 5. Rate Pressure Pressure (RPP) after the Circuit (C) and Multiple Sets (MS) Methods. Values Figure 5. Rate pressure product (RPP) after circuit (C) and multiple sets (MS) methods. Values were obtained at were rest Obtained and 90 minutes at Rest after and the for exercise 90 min protocol, after the at Exercise 15-minute Protocol intervals. at Mean 15-min values Intervals. are presented. Mean values are *Significant difference compared to rest, p<0.05. a Significant difference compared to the MS method, p<0.05. shown. *Significant difference compared to rest, P<0.05. a Significant difference compared to the MS method, P<0.05.

10 45 DISCUSSION The main findings of this study are in normotensive adult males: (a) both the C and MS sessions resulted in similar PEH responses; (b) autonomic changes after RE were similar for the C and MS sessions; and (c) after a session of RE, a predominance of sympathetic activity is shown with a consequent rise in HR. Our results are consistent with the majority of the published articles employing C training sessions (3,17,18) and MS sessions (10,18-21). However, the post-exercise hypotensive response of SBP and DBP observed in this study were slightly higher in magnitude than those reported previously (mean reduction of 5.0% [6.18 ± 7.38 mmhg] in SBP and 7.7% [6.34 ± 4.89 mmhg] in DPB after the MS method and 5.1% [6.22 ± 8.85 mmhg] in SBP and 7.6% [6.38 ± 5.43 mmhg] in DBP after the C method). These values indicate that the PEH after RE in normotensive adults was similar to that which occurs in hypertensive patients. Thus, these findings indicate that RE can be a very important tool in the treatment and prevention of elevated blood pressure. To our knowledge, the present study is the first to analyze the effect of C and MS sessions, with the same total work performed on the hypotensive response and HR variability together. We hypothesized that the absence of rest interval between sets and exercises of the C versus the MS session could influence PEH. Despite that, the results were similar for almost all time points of BP monitoring. Both methods led to a reduction of SBP, a significant difference between the two was observed only in the first minutes after completing the exercise session (i.e., 0 min and 15 min). The difference between the SBP values for the two different training sessions at postexercise time points was negligible, ranging from 0.5% to 3.5%. Both sessions resulted in a significant hypotensive response from 15 to 90 min post-exercise, except for the C session at 60 min post-exercise. The significant increase in BP at 0 min post-exercise shown after the C session is probably due to the short rest period of 30 sec between sets and exercises that would increase cardiovascular stress during the session. The difference in DBP at the post-exercise time points was also low, ranging from 0.22% to 2.40%. Both the C and MS sessions caused a significant reduction in DBP immediately after exercise with the post-exercise hypotensive response lasting 75 min for the C session and up to 90 min for the MS session. There were no significant differences between the methods at any post-exercise time point. The post-exercise hypotensive MAP response was similar for the C and MS sessions. Both sessions showed a significant hypotensive response from 15 to 90 min post-exercise with the MS sessions also showing a hypotensive response at 0 min post-exercise. Thus, both the C and the MS resistance training session resulted in similar and significant post-exercise hypotensive responses. In the present study, sessions of RE were performed using a total of 12 exercises for all muscle groups of the body (chest, back, legs, abdominal, and lumbar), in accordance with the American College of Sports Medicine recommendations for clinically healthy, sedentary

11 adults (1). However, the isolated effect of the exercise over the PEH seems to be dependent on other variables, such as intensity (22) or monitoring period (23). Although we are not aware of any other studies comparing PEH and HRV between C and MS resistance training sessions, some studies have analyzed the post-exercise BP response after other methods of RE and multiple-set RE. Rodriguez et al. (9) compared one MS with a tri-set session (TRI). The TRI session consisted of performing three exercises for the same muscle group in sequence without a rest period between exercises (3 sets of 10 reps with 70% of 1RM). Between each TRI sequence, there was a 1 min rest interval. The MS group performed 3 sets of 10 reps for the same exercises, but with 1 min rest interval between sets and exercises. The authors hypothesized that the TRI session would cause greater stress on the cardiovascular system and, consequently, a PEH response of magnitude and/or duration. However, a PEH response was not demonstrated in either session, which suggests that the performance of only upper body exercises, (six exercises for the pectoral and dorsal muscle groups) and no exercises for the legs (major muscle group) may be responsible for the results. It is important to note that the rest interval length also seems not to influence the PEH response (24). Thus, the PEH may be dependent on endothelial vasodilator release, such as nitric oxide, prostaglandins, and adenosine, which is related to the higher rates and efforts involving major muscle groups (8,25). By contrast, Simão et al. (33) examined the PEH response with 6 exercises (MS; 6 exercises, 3 sets with 6 maximum reps (RM) load and C; 6 exercises, 3 sets of 12 reps with 50% of 6 RM load), but also included exercises for the major muscle groups, such as the legs. Blood pressure was recorded for 60 min after the RE sessions. PEH occurred after both of the experimental sessions, but only for SBP and for a short period of time post-exercise of 0 to 50 min after the MS session and from 0 to 40 min after the C session. In contrast, Hill and colleagues (18) evaluated the effect of three cycles of C training that involved 4 exercises executed to voluntary fatigue (3 sets with a load of 70% 1RM and 30-sec interval between exercises) on the PEH in normotensive subjects and found that SBP PEH response remained unchanged during the 60 min of recovery, but the subjects DBP PEH was slightly lower than before exercise. Bermudez et al. (3) also examined the PEH response from a circuit RE session in normotensive adults. The circuit consisted of 3 sets of 10 exercises with an average of 23 reps per set at an estimated intensity of 40% 1RM, 30-sec rest periods between exercises and 2 min of rest between each complete circuit. The results showed a single session of RE in normotensive subjects was enough to promote significant reductions in both SBP and DBP levels during sleep after exercise. In agreement, Fisher (13) studied normotensive and hypertensive women after 3 sets of 5 RE exercises performed in a circuit at 50% 1RM of which the subjects blood pressure (SBP, DBP, and MBP) was monitored during the 60 min after the exercise session. The results showed a SBP PEH response during 60 min after exercise. The C and MS sessions also showed a similar post-exercise HRV response. Both RE sessions showed a significant decrease in the RR interval, increase in LF, decrease in HF, and an increase in the LF/HF ratio for the entire post-exercise period observed with no significant differences between sessions at any time point. Although a PEH response was 46

12 shown in both sessions, the aforementioned HRV characteristics indicate a predominance of sympathetic activity in relation to rest and a decrease of sympathetic activity as the postexercise time increased for both RE sessions. However, the numerous variables that comprise an RE session (intensity, volume, resistance type, order and selection of exercises, time under tension, and equipment) have been shown to influence the behavior of the cardiac autonomic system (11,12,27). Thus, there seems to be little known concerning the effects of the variables of RE on cardiac autonomic behavior. It is difficult to compare the present results with other studies due to the small number of studies that examined the effect of a complete RE session on PEH and HRV. In a review by Cardozo and colleagues (8), only one study was found on the mechanisms responsible for PEH in normotensive subjects. This study showed a reduction in cardiac output due to a decrease in stroke volume, which was probably due to a reduction in the ventricular pre-load. Recently, Queiroz et al (28) also described the same behavior after 3 sets of reps until moderate fatigue (slowing of movement) in RE (50% of 1 RM, intervals between sets and exercises = 90 sec). Regarding the HRV, other studies have also observed the same pattern of response to RE observed in the present study. Maior et al. (23) compared two RE sessions with different intensities (6RM vs. 12RM). Their findings indicate a decrease in the HRV parameters related predominantly to the activity of the parasympathetic nervous system (PNS) and an increase in the activity related to sympathetic nervous system (SNS). Rezk et al. (30) compared training sessions conducted at 40% and 80% of 1RM and found that the increase in the observed HR was the result of an increase in the SNS activity and a decrease in the parasympathetic modulation to the heart. The behavior of the CNS appears to be influenced by a reduction in plasma volume due to its influx into the interstitial space (29), thus promoting a reduction in cardiac output and a decrease in venous return. These adjustments result in deactivation of cardiopulmonary receptors and a subsequent increase in heart rate (11). According to Buchheit et al. (6) and Rezk et al (30), the change in plasma volume may partially explain the behavior of HRV. Buchheit et al. (6) suggest that the alteration of the arterial baroreceptors (that affect cardiac control) is dependent on the levels of atrial pressure and stroke volume. A decrease in plasma volume can cause an inhibitory influence on the receptors of the parasympathetic cardiovascular control centers in the medulla and followed by CNS excitatory effect on SNS (5) and HR, although the PEH still occurs. In general, we found that both the C and MS sessions in normotensive subjects showed a significant acute reduction in BP post-exercise. This reduction in BP can be considered clinically relevant, especially regarding normotensive adults and may contribute to strengthening the evidence that for middle-aged normotensive individuals, RE is not only a instrument of preventing age-related disease and degeneration such as osteoporosis and sarcopenia, reduced functional capacity, and incidence of falls (19,31), but also a tool for the maintenance of cardiovascular health and prevention of chronic degenerative diseases related to increased blood pressure. 47

13 This study population was chosen to represent the greatest number of RE practitioners, and yet few scientific studies have been produced relating to the application of RE for this group. Furthermore, supposedly a sample of normotensive individuals still have the cardiovascular regulatory mechanisms preserved, allowing the observation of the influence of the RE on the CNS, without the influence of pathological processes. Thus, we could infer that the changes in subjects behavior were triggered by the effect of exercise without the influence of any type of disability or deterioration in cardiovascular functioning. Notably, moderate pressure overload can be beneficial from the point of view of prophylaxis (32), including treatment of people with cardiovascular disease and chronic users of antihypertensive medication (29,33). Some studies have reported that coronary heart disease patients under pharmacological treatment after performing RE of moderate intensity improve the function of the left ventricle, especially subjects ejection fraction (34,35). CONCLUSION Circuit and multiple-sets resistance exercises promote a systolic and diastolic post-exercise hypotension in normotensive subjects despite the difference in total time of the exercise session. For both RE methods there was an increase in HR that was probably promoted by the activation of sympathetic (LF of HRV) and deactivation of parasympathetic (HF of HRV) modulation of the heart that remained impaired until 90 min post-exercise. 48 Address for correspondence: Daniel Rodriguez, Faculty of Physical Education - University São Judas Tadeu. São Paulo / SP Brazil, d-rodriguez@uol.com.br REFERENCES 1. American College of Sports Medicine. Progression models in resistance training for healthy adults. Med Sci Sports Exerc. 2009;34: American Heart Association. Resistance exercise in individuals with and without cardiovascular disease; 2007 update: A Scientific Statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism. Circ. 2007;116: Beck DT, Casey DP, Martin JS, Emerson BD, Braith RW. Exercise training improves endothelial function in young prehypertensives. Exp Biol Med. 2013;238(4): Bermudes AM, Vassallo DV, Vasquez EC, Lima EG. Ambulatory blood pressure monitoring in normotensive individuals undergoing two single exercise sessions: Resistive exercise training and aerobic exercise training. Arq Bras Cardiol. 2004;82:

14 5. Brito Ade F, de Oliveira CV, Santos Mdo S, Santos Ada C. High-intensity exercise promotes postexercise hypotension greater than moderate intensity in elderly hypertensive individuals. Clin Physiol Funct Imaging. 2014;34(2): Buchheit M, Laursen PB, Al Haddad H, Ahmaidi S. Exercise-induced plasma volume expansion and post-exercise parasympathetic reactivivation. Eur J Appl Physiol. 2009;105: Bush JA, Kraemer WJ, Mastro AM, Triplett-McBride NT, Volek JS, Putukian M, Sebastianelli WJ, Knuttgen HG. Exercise and recovery responses of adrenal medullary neurohormones to heavy resistance exercise. Med Sci in Sport Exerc. 1999;31-4: Cardoso Jr CG, Gomides RS, Queiroz ACC, Pinto LG, Lobo FS, T Tinucci, Mion Jr D, Forjaz CLM. Acute and chronic effects of aerobic and resistance exercise on ambulatory blood pressure. Clinics. 2010;65(3): Chen CY, Bonham AC. Post exercise hypotension: Central mechanisms. Exerc Sport Sci Rev. 2010;38(3): De Sousa NM, Magosso RF, Dipp T, Plentz RD, Marson RA, Montagnolli AN, Martins RA, Perez SE, Baldissera V. Continuous blood pressure response at different intensities in leg press exercise. Eur J Prev Cardiol. 2014;21(11): Duncan MJ, Birch SL, Oxford SW. The effect of exercise intensity on post resistance exercise hypotension in trained men. J Strength Cond Res. 2014;28(6): European Society of Cardiology. Task Force of the European Society of Cardiology and The North American Society of Pacing and Electrophysiology. Heart rate variability standards of measurement, physiological interpretation, and clinical use. Eur Heart J. 1996;17: Fisher MM. The effect of resistance exercise on recovery blood pressure in normotensive and borderline hypertensive women. J Strength Cond Res. 2001;15: Focht BC, Koltyn KF. Influence of resistance exercise of different intensities on state anxiety and blood pressure. Med Sci Sports Exerc. 1999;31(3): Gjovaag T, Hjelmeland AK, Øygard JB, Vikne H, Mirtaheri P. Resistance exercise and acute blood pressure responses. J Sports Med Phys Fitness. 2015;20. [Epub ahead of print]. 16. Goto C, Higashi Y, Kimura M, Noma K, Hara K, Nakagawa K, et al. Effect of different intensities of exercise on endothelium-dependent vasodilation in humans: Role of endothelium-dependent nitric oxide and oxidative stress. Circ. 2003;108:

15 17. Haskell WL, Lee IM, Pate RR, Powell KE, Blair SN, Franklin BA, Macera CA, Heath GW, Thompson PD, Bauman A. Physical activity and public health: Update recommendation for adults from the American College of Sports and Medicine and the American Heart Association. Circ. 2007;116: Hill DW, Collins MA, Cureton KJ, Demello JJ. Blood pressure response after weight training exercise. J Appl Sport Sci Res. 1989;3: Iglesias-Soler E, Boullosa DA, Carballeira E, Sánchez-Otero T, Mayo X, Castro-Gacio X, Dopico X. Effect of set configuration on hemodynamics and cardiac autonomic modulation after high-intensity squat exercise. Clin Physiol Funct Imaging. 2014;29. DOI: /cpf [Epub ahead of print]. 20. Jones H, Atkinson G, George K, Edwards B. Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done? Eur J Appl Physiol. 2007;102: Kraemer WJ, Fry AC. Strength testing: Development and evaluation of methodology. In: Maud PJ, Foster C. Physiological Assessments of Human Fitness (pp ). Champaign, IL: Human Kinetics, Lima AHRA, Forjaz CLM, Silva GQM, Meneses AL, Silva AJMR, Ritti-Dias MR. Acute effect of resistance exercise intensity in cardiac autonomic modulation after the exercise. Arq Bras Cardiol. 2011;96(6): Maior AS, Netto CF, Eichwald A, Druck G, Villaça G, Foschiera RS, Oliveira WB, Menezes P, Marques-Neto SR, Cavinato C. Influência da intensidade e do volume de treinamento resistido no comportamento autonômico cardíaco. Rev SOCERJ. 2009; 22(4): Marchionni N, Fattirolli F, Fumagalli S, Oldridge N, Del Lungo F, Morosi L, et al. Improved exercise tolerance and quality of life with cardiac rehabilitation of older patients after myocardial infarction: Results of a randomized, controlled trial. Circ. 2003;107(17): Marques EA1, Mota J, Viana JL, Tuna D, Figueiredo P, Guimarães JT, Carvalho J. Response of bone mineral density, inflammatory cytokines, and biochemical bone markers to a 32-week combined loading exercise programme in older men and women. Arch Gerontol Geriatr. 2013;57(2): Moreira SR, Lima RM, Silva KE, Simões HG. Combined exercise circuit session acutely attenuates stress-induced blood pressure reactivity in healthy adults. Braz J Phys Ther. 2014;18(1): Polito MD, Farinatti PTV. Blood pressure behavior after counter-resistance exercises: A systematic review on determining variables and possible mechanisms. Rev Bras Med Esporte. 2006;12(6):345e-350e. 50

16 28. Queiroz AC, Gagliardi JFL, Forjaz CLM, Rezk CC. Clinic and ambulatory blood pressure responses after resistance exercise. J Strength Cond Res. 2009;23: Queiroz AC, Sousa JC, Cavalli AA, Silva ND Jr, Costa LA, Tobaldini E, Montano N, Silva GV, Ortega K, Mion D Jr, Tinucci T, Forjaz CL. Post-resistance exercise hemodynamic and autonomic responses: Comparison between normotensive and hypertensive men. Scand J Med Sci Sports DOI: /sms [Epub ahead of print]. 30. Rezk CC, Marrache RCB, Tinucci T, Mion Jr D. Forjaz CLM. Post-resistance exercise hypotension, hemodynamics, and heart rate variability: Infuence of exercise intensity. Eur J Appl Physiol. 2006;98: Rodriguez D, Polito MD, Bacurau RFP, Prestes J, Pontes Jr FL. Effect of different resistance exercise methods on post-exercise blood pressure. Int J Exerc Sci. 2008: 1(4): Sharman JE, La Gerche A, Coombes JS. Exercise and cardiovascular risk in patients with hypertension. Am J Hypertens. 2015;28(2): Simão R, Fleck S, Polito MD, Monteiro WD, Farinatti PTV. Effects of resistance training intensity, volume, and session format on the postexercise hypotensive response. J Strength Cond Res. 2005;19: Veloso J, Polito MD, Riera T, Celes R, Vidal JC, Bottaro M. Effects of rest interval between exercise sets on blood pressure after resistance exercises. Arq Bras Cardiol. 2010;94(4): The opinions expressed in JEPonline are those of the authors and are not attributable to JEPonline, the editorial staff or the ASEP organization.

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