Post-exercise hypotension (PEH), the reduction of blood pressure (BP) after a single bout of exercise, is of great clinical relevance. As the magnitude of this phenomenon seems to be dependent on pre-exercise BP values and chronic exercise training in hypertensive individuals leads to BP reduction; PEH could be attenuated in this context. Therefore, the aim of the present study was to investigate whether PEH remains constant after resistance exercise training. Fifteen hypertensive individuals (46±8 years; 88±16 kg; 30±6% body fat; 150±13/93±5 mm Hg systolic/diastolic BP, SBP/DBP) were withdrawn from medication and performed 12 weeks of moderate-intensity resistance training. Parameters of cardiovascular function were evaluated before and after the training period. Before the training program, hypertensive volunteers showed significant PEH. After an acute moderate-intensity resistance exercise session with three sets of 12 repetitions (60% of one repetition maximum) and a total of seven exercises, BP was reduced post-exercise (45–60 min) by an average of aproximately −22 mm Hg for SBP, −8 mm Hg for DBP and −13 mm Hg for mean arterial pressure (P<0.05). However, this acute hypotensive effect did not occur after the 12 weeks of training (P>0.05). In conclusion, our data demonstrate that PEH, following an acute exercise session, can indeed be attenuated after 12 weeks of training in hypertensive stage 1 patients not using antihypertensive medication.
Post-exercise hypotension (PEH) is a reduction in blood pressure (BP) observed after a single bout of exercise.1, 2 Most previous studies regarding PEH have been performed with an aerobic exercise design.3, 4 However, resistance exercise training (RET) is also considered as an important contribution to exercise training programs for hypertensive individuals.5, 6, 7, 8
PEH could be clinically relevant, because it would mantain BP of hypertensinve individuals transiently at lower levels during day-time intervals, when BP is typically at its highest levels.2 Despite PEH being considered clinically relevant for BP control both in normotensive and hypertensive individuals,9, 10, 11 there is a lack of data regarding whether PEH would still be observed in hypertensive individuals after physical conditioning programs, specially in RET programs.5, 12 PEH has been documented to be greater in hypertensive than normotensive individuals5 and its magnitude seems to be dependent on resting/pre-exercise BP values.13, 14 As chronic exercise induces resting BP reduction, it is possible that the magnitude of PEH can be reduced due to adaptation to exercise.5, 15 This issue has been poorly investigated, especially with regards to resistance exercise,16 and has not been evaluated in hypertensive individuals submitted to RET. Therefore, the aim of the present study was to investigate whether PEH would be attenuated after 12 weeks of resistance exercise in medically-supervised hypertensive individuals who are not under antihypertensive medication.
Patients and methods
A total of 15 sedentary (less than 2 h per week of physical activity), middle-aged adult males (46±8 years), with diagnosis of hypertension (defined as mean resting systolic BP (SBP) between 140 and 159 mm Hg and mean resting diastolic BP (DBP) between 90 and 99 mm Hg), corresponding to stage 1 hypertension according to the American Heart Association, were recruited via advertisements from a local cardiology clinic (Mogi das Cruzes, São Paulo, SP, Brazil).17 Individuals with physical disabilities, diabetes, cardiac arrhythmias, end-organ injury, peripheral arterial disease, myocardial infarction, stroke, coronary heart disease, heart failure or a recent history of smoking or drug/alcohol abuse were excluded from the trial. All volunteers gave their informed written consent before participation. The Ethics Committee of the Federal University of Sao Paulo, SP, Brazil, approved the experimental procedures (0564/09). Before and during the trial, patients were excluded for the following reasons: 1st phase: randomized recruiting through advertisements (n=25). Excluded: arrhythmia (n=2), diabetes (n=1); 2nd phase: medication washout and test exercise period (n=22). Excluded: BP <140/90 mm Hg (n=3), BP⩾180/100 mm Hg (n=2), back pain after exercise (n=1); 3rd phase: 12-week resistance training (n=16). Excluded: training program not completed (n=1).
Medication washout period
Eleven of the volunteers were under antihypertensive medication for an average of 6±2 years before the beginning of the study. These volunteers were first submitted to a 6-week medication washout period. All antihypertensive medications such as calcium blockers, ACE inhibitors or angiotensin II type-1 receptor blockers were gradually withdrawn during the first 2 weeks of the washout period. After 2 weeks without antihypertensive medication, the BP of the volunteers reached values equivalent to stage 1 hypertension, according to the norms from the American Heart Association.17, 18 All types of non-antihypertensive medication was additionally avoided for at least 1 week before the first tests. The other four volunteers never used any anti-hypertensive medications before the trial. They were examined weekly and were required to have between 140–159 mm Hg for SBP or 90–99 mm Hg for DBP during two consecutive visits and an average BP in this range across four visits. All subjects were routinely medically supervised during the experimental period.
Exercise testing protocol
All voluntaries were submitted to a maximal treadmill walking test, using the modified Balke protocol.19 A 12-lead electrocardiograph (model SM 400; TEB, New York, NY, USA) was used to record the maximal heart rate (HR) and to rule out cardiovascular diseases. Arterial BP was measured during the test by using a sphygmomanometer (BP cuff) and stethoscope (Becton Dickinson, New York, NY, USA). Participants were excluded in case of ST-segment depression greater than 1 mm, complex arrhythmias, or when ischemic symptoms were observed during exercise testing.
Body composition was determined using the Jackson and Pollock seven sites skinfold protocol.20 Skinfold thickness was measured at seven sites: sub-scapular, triceps, biceps, chest, abdomen, thigh and supra-iliac, by Lange skinfold calipers (Beta Technology Inc, Santa Cruz, CA, USA). Three measurements were made of each skinfold and the average value was used to calculate body composition.
Assessment of muscle strength
Maximal isotonic voluntary contractile strength was assessed for seven distinct muscle groups, using the one-repetition-maximum technique (1-RM, that is, the weight that can be lifted no more than once) and pinloaded weight-stack resistance equipment (Biotech, São Paulo, Brazil), with minimum 2-kg increments, that was also used during the exercise-training program. To maintain the proper strength of 60% 1-RM and to assess the strength gain, the maximal isotonic voluntary contractile strength assessment was performed on three occasions: at baseline, during the 6th week of training (at the middle of the RET program), and 24 h after the last training session of the RET program (that is, during the 12th week). Before the test, subjects underwent three familiarization sessions (two sets, 12 repetitions of each exercise with the minimum weight allowed by the machines) on non-consecutive days. Following a brief warm-up, seven resistance exercises were used during the 1-RM test, which consisted of: (i) leg press, (ii) leg curl, (iii) chest press, (iv) lat pulldown, (v) shoulder press, (vi) biceps curl and (vii) triceps extension. Subjects were instructed in correct-lifting and hand-gripping techniques according to the norms of the National Strength and Conditioning Association (USA).21
Resistance exercise training (RET)
All volunteers were instructed 1 week before training on the techniques involved in the different RET bouts and on how BP would be measured. Subjects were also familiarized with the laboratory environment. During the tests, the air temperature was kept stabilized between 21 and 24 °C and relative humidity ranging between 50–60%. No dietary advice was provided, and participants were asked to maintain their normal caloric intake during the study. Participants were instructed to refrain from any other regular exercise during all of the entire study period. The 12-week RET consisted of three weekly sessions on non-consecutive days of 1 h of conventional (non-circuited) strength training in a gym (Trainer Gym, Mogi das Cruzes, SP, Brazil). RET was performed at 60% of 1-RM in three consecutive sets of 12 repetitions of the following seven exercises: (i) leg press, (ii) leg curl, (iii) chest press, (iv) lat pulldown, (v) shoulder press, (vi) biceps curl and (vii) triceps extension, with 2 min pauses between the sets (average time of each set: 36 s) and 1 min pauses between the exercises (total exercise session approximately 45 min), following the conventional training model in the American College of Sports Medicine Guidelines.22 In addition, subjects were requested to exhale air during the most strenuous phase of the repetition and to inhale it during the less strenuous phase of the repetition. The weight was increased by approximately 5 kg when the subject could successfully complete more than 12 repetitions in a proper manner. The RET sessions were held in the afternoon between 1300 and 1600 h and were supervised by trained exercise physiologists who directed each stage of the session, instructing the subjects about what should be performed.
Blood pressure and heart rate
SBP, DBP and mean arterial BP (MAP=DBP+ (SBP−DBP)/3), as well as HR and pulse pressure (PP=SBP−DBP) were measured before, during and immediately after each training session of the RET program (automated non-invasive BP monitor Microlife 3AC1-1PC, Microlife AG, Widnau, Switzerland).23 Rate-pressure product (RPP) was evaluated as RPP=HR × SBP. The measurement during the training session was performed after the subjects completed the fourth exercise (in a total of seven); the objective of this measurement was to guarantee that BP did not fall during the training session.5 All BP measurements were taken on the left arm. Individual cuffs were labeled with the ranges of arm circumferences.18 Pre-exercise BP did not exceed 160 and 100 mm Hg for SBP and DBP, respectively. All measurements were done by the same investigator (MRM).
Evaluation of post exercise hypotension (RES)
A period of 72 h after the end of the medication washout period, the subjects were submitted to an experimental resistance exercise session (RES) to investigate the occurrence of PEH. The same experimental exercise test was repeated 72 h after finishing the last training session of the 12-week RET program. Upon arrival in the laboratory (between 1300 and 1600 h) after a light standard meal, subjects remained resting in supine position for 20 min before starting the exercise. Subjects did not perform any physical activity for at least 24 h before the evaluations and avoided caffeine or alcohol. During exercise, subjects received 15 ml of water per kg of body weight to replace water loss due to sweating. The equipment and the training protocol used were exactly the same as in the RET program (see above). The load lifted (60% 1-RM) was adjusted by means of the 1-RM test, carried out at baseline and after 12 weeks of training. To evaluate the occurrence of PEH, BP and HR were additionally measured in the supine position (resting), 5, 10, 15, 30, 45 and 60 min after completing the acute RES.
Analysis of variance with repeated measurements (group, treatment and time interaction) was used for statistical analyses, and the Tukey post-hoc test was used to identify significant data points (P<0.05). All pre- and post-comparisons were performed using the Student's t-test. Statistical analyses were performed using the Prism 5 software package. Differences were considered significant for P<0.05. Data are expressed as mean±s.d.
Table 1 shows the anthropometric characteristics of the hypertensive volunteers before and after 12 weeks of the RET program. There was an increase in lean muscle mass (P<0.01), with a reduction in total fat mass and fat mass percentage (P<0.001), without any significant change in total body weight (P>0.05).
Blood pressure–resistance exercise training (RET)
The results indicate that 12 weeks of RET had a significant effect on baseline BP (Table 2). RET decreased mean resting SBP (150±3 to 134±3 mm Hg, P<0.001), DBP (93±2 to 81±1 mm Hg, P<0.01) and MAP (112±2 to 99±3 mm Hg, P<0.01).
Evaluation of PEH (RES)
Before the beginning of the RET program, SBP, DBP and MAP of the hypertensive subjects submitted to an acute resistance exercise bout were significantly reduced 45 min after the RES effort (Figures 1, 2 and 3 for SBP, DBP and MAP, respectively). However, when we evaluated the subjects for PEH after the 12 week of RET program (Figures 1,2,3), when the hypertensive volunteer's baseline BP was ‘normalized’ by the RET, we detected no significant changes in BP 45 min after the acute resistance exercise bout. These results indicate that PEH was attenuated by the 12 weeks of RET program.
Rate-pressure product-resistance exercise training
A significant reduction of the RPP after 12 weeks of RET could be observed (Table 2).
Rate-pressure product-resistance exercise session
The RPP was measured up to 1 h after the acute RES in the volunteers in two different conditions, before and after the RET program. A significant reduction of RPP 15–60 min after the RES could be observed in the subjects before the RET program. Twelve weeks later, the reduction in RPP could not be observed after the acute RES (Figure 4).
No significant differences in pulse pressure concerning resistance exercise were observed before versus after 12 weeks of training (Table 2).
In the last few years, the potential clinical benefits of PEH to hypertensive individuals have captured the attention of several investigators.2, 5, 24 Attempting to demonstrate the relevance of PEH for the treatment of hypertensive individuals, some criteria such as the magnitude of BP reduction, the duration of PEH and its occurrence outside of the laboratory have been investigated.1, 2, 3, 10
Here we evaluated the PEH of hypertensive individuals before and after 12 weeks of a moderate-intensity RET program. Our primary new finding is that stage 1 hypertensives submitted to an acute experimental resistance exercise bout show attenuated PEH after the 12-week RET program.
In the present study, our initial working hypothesis was that PEH would be reduced/suppressed after chronic adaptation induced by an exercise program.12 In this context, the suppression of PEH observed in our subjects seems to follow exactly this proposition, as our training protocol elicited a significant reduction in resting BP (SBP, DBP and MAP), and RPP. However, our results do not provide us with insight into potential mechanisms that could be involved in the attenuation of PEH. Interestingly, several reports on PEH in sedentary individuals led Hamer12 to hypothesize that PEH has no role in the anti-hypertensive effect of training. Our results could suggest that neurohumoral (for example, sympathetic nerve activity) or structural (for example, vascular) adaptations known to be induced by RET7 are involved in a gradual reduction of PEH. In this sense, it would be interesting to investigate if the reduction of PEH could be used as an indicator that individuals have adapted to resistance exercise.
It is interesting to note that the reduced incidence of hypertension associated with activity and fitness has been attributed to both the chronic adaptation promoted by exercise training and the reduction of resting BP following an acute exercise bout.12 The clinical relevance of PEH would then be related to maintaining lower levels of BP during day-time intervals when BP is typically at its highest levels.2 This role is however not supported directly by our data. On the other hand, it is interesting to note that some adaptations promoted by RET have been the subject of concern. In opposition to high-intensity RET, moderate habitual RET neither reduced central arterial compliance nor altered arterial stiffness.25 Finally, the absence of PEH could make the design of RET programs easier, as only chronic adaptation and not temporal BP reduction would become the objective of these programs.
To date, we are unaware of any study that has investigated the RPP after resistance exercise (acute/chronic) in hypertensive patients not under anti-hypertensive medication. Before the RET program, there was a significant decrease in RPP after 15 min of a RE bout. This decrease was maintained for more then 45 min. After 12 weeks of RET program, there was a decrease of approximately 15% of the RPP. This reduction of RPP was mediated by the reduction of SBP, as no significant changes in HR were observed (data not show). These statistically significant reductions are clinically important, because several studies have shown that both cardiovascular morbidity and mortality increase with increasing RPP in patients with hypertension.26
Previous researchers have indicated that the pre-exercise degree of hypertension is a more important moderator of PEH than age, body mass index, waist circumference and maximal oxygen update.5 We observed a significant increase in muscle mass and decreased fat mass after 12 weeks of training. However, there was no correlation of these values with PEH. Likewise, MacDonald et al.27 concluded that the mass of the working muscle does not directly affect the magnitude of PEH.
We are aware of only one study investigating the influence of training conditions on PEH. Senitko et al.28 demonstrated that trained individuals present PEH in the same magnitude as untrained individuals. Unfortunately, methodological differences, for example, the fact that sedentary/trained-normotensive individuals were submitted to acute exhaustive aerobic exercise, compromise an eventual comparison between these results and ours.28
It is worth mentioning that our methodology does not permit us to determine the minimal training interval during the weeks that attenuated PEH. That is, it is possible that hypertensive individuals who perform less intense and/or frequent exercise are able to continue presenting BP reduction after exercise. On the other hand, the acute resistance exercise effect may reduce BP in a cumulative yet diminishing manner so that subsequent sessions result by compensation mechanisms in asymptotically smaller PEH.15, 29
However, considering that our results support the hypothesis that PEH is possibly related to BP reductions induced by chronic exercise, it could be expected that the persistence of PEH would in theory be observable in individuals that are not completely adapted to a chronic exercise program. This is a very important issue for professionals involved in healthcare, who prescribe exercise, and needs to be further investigated in future studies. A second limitation of our study is the small sample size and the fact that only male subjects participated in the study, although evidence suggests that PEH is gender independent.2
In conclusion, our data demonstrate that PEH after a single RES can be attenuated by chronic moderate-intensity resistance exercise. As far as we know, this is the first study that investigated the role of physical training on PEH of hypertensive individuals.
Kenney MJ, Seals DR . Postexercise hypotension. Key features, mechanisms, and clinical significance. Hypertension 1993; 22: 653–664.
MacDonald JR . Potential causes, mechanisms, and implications of post exercise hypotension. J Hum Hypertens 2002; 16: 225–236.
Motta DF, Lima LC, Arsa G, Russo PS, Sales MM, Moreira SR et al. Effect of type 2 diabetes on plasma kallikrein activity after physical exercise and its relationship to post-exercise hypotension. Diabetes Metab 2010; 36: 363–368.
Pontes Jr FL, Bacurau RF, Moraes MR, Navarro F, Casarini DE, Pesquero JL et al. Kallikrein kinin system activation in post-exercise hypotension in water running of hypertensive volunteers. Int Immunopharmacol 2008; 8: 261–266.
Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA . American College of Sports Medicine position stand. Exercise and hypertension. American College of Sports Medicine. Med Sci Sports Exerc 2004; 36: 533–553.
Cornelissen VA, Fagard RH . Effect of resistance training on resting blood pressure: a meta-analysis of randomized controlled trials. J Hypertens 2005; 23: 251–259.
Collier SR, Kanaley JA, Carhart Jr R, Frechette V, Tobin MM, Hall AK et al. Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives. J Hum Hypertens 2008; 22: 678–686.
Williams MA, Haskell WL, Ades PA, Amsterdam EA, Bittner V, Franklin BA et al. 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. Circulation 2007; 116: 572–584.
Moraes MR, Bacurau RFP, Ramalho JD, Reis FC, Casarini DE, Chagas JR et al. Increase in kinins on post-exercise hypotension in normotensive and hypertensive volunteers. Biol Chem 2007; 388: 533–540.
Mota MR, Pardono E, Lima LC, Arsa G, Bottaro M, Campbell CS et al. Effects of treadmill running and resistance exercises on lowering blood pressure during the daily work of hypertensive subjects. J Strength Cond Res 2009; 23: 2331–2338.
Melo CM, Alencar Filho AC, Tinucci T, Mion Jr D, Forjaz CL . Postexercise hypotension induced by low-intensity resistance exercise in hypertensive women receiving captopril. Blood Press Monit 2006; 11: 183–189.
Hamer M . The anti-hypertensive effects of exercise: integrating acute and chronic mechanisms. Sports Med 2006; 36: 109–116.
Atkinson G, Cable NT, George K . The relationship between baseline blood pressure and magnitude of postexercise hypotension. J Hypertens 2005; 23: 1271–1272.
Taylor CE, Jones H, Zaregarizi M, Cable NT, George KP, Atkinson G . Blood pressure status and post-exercise hypotension: an example of a spurious correlation in hypertension research? J Hum Hypertens 2010; 24: 585–592.
Nobrega AC . The subacute effects of exercise: concept, characteristics, and clinical implications. Exerc Sport Sci Rev 2005; 33: 84–87.
MacDonald JR, MacDougall JD, Interisano SA, Smith KM, McCartney N, Moroz JS et al. Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise. Eur J Appl Physiol Occup Physiol 1999; 79: 148–154.
Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289: 2560–2572.
Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN et al. Recommendations for blood pressure measurement in humans and experimental animals: part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Circulation 2005; 111: 697–716.
Josephson RA, Shefrin E, Lakatta EG, Brant LJ, Fleg JL . Can serial exercise testing improve the prediction of coronary events in asymptomatic individuals? Circulation 1990; 81: 21–24.
Pollock ML, Jackson AS . Research progress in validation of clinical methods of assessing body composition. Med Sci Sports Exerc 1984; 16: 606–615.
Armstrong LE, Whaley MH, Brubaker PH, Otto R . Health-related physical fitness testing and interpretation. In: Whaley MH, Brubaker PH, Otto RM (eds). ACSM's Guidelines for Exercise Testing and Prescription. 7th edn. Lippincott Williams & Wilkins: Philadelphia, PA, 2006, pp 62–64.
American College of Sports Medicine. American College of Sports Medicine position stand. Progression models in resistance training for healthy adults. Med Sci Sports Exerc 2009; 41: 687–708.
Topouchian JA, El Assaad MA, Orobinskaia LV, El Feghali RN, Asmar RG . Validation of two devices for self-measurement of brachial blood pressure according to the International Protocol of the European Society of Hypertension: the SEINEX SE-9400 and the Microlife BP 3AC1-1. Blood Press Monit 2005; 10: 325–331.
Halliwill JR . Mechanisms and clinical implications of post-exercise hypotension in humans. Exerc Sport Sci Rev 2001; 29: 65–70.
Okamoto T, Masuhara M, Ikuta K . Effect of low-intensity resistance training on arterial function. Eur J Appl Physiol 2010; 111: 743–748.
White WB . Heart rate and the rate-pressure product as determinants of cardiovascular risk in patients with hypertension. Am J Hypertens 1999; 12: 50S–55S.
MacDonald JR, MacDougall JD, Hogben CD . The effects of exercising muscle mass on post exercise hypotension. J Hum Hypertens 2000; 14: 317–320.
Senitko AN, Charkoudian N, Halliwill JR . Influence of endurance exercise training status and gender on postexercise hypotension. J Appl Physiol 2002; 92: 2368–2374.
Thompson PD, Crouse SF, Goodpaster B, Kelley D, Moyna N, Pescatello L . The acute versus the chronic response to exercise. Med Sci Sports Exerc 2001; 33: S438–S445.
We thank cardiologists Dr Ricardo Harada and Dr Manoel Leitão Neto for assistance. We additionally acknowledge the Salvape and the Trainer Gym, Mogi das Cruzes. This study was supported by grants from Fundação de Amparo à Pesquisa do Estado de São Paulo-FAPESP (06/59081-6) and Conselho Nacional de Pesquisa e Tecnologia-CNPq.
The authors declare no conflict of interest.
About this article
Cite this article
Moraes, M., Bacurau, R., Simões, H. et al. Effect of 12 weeks of resistance exercise on post-exercise hypotension in stage 1 hypertensive individuals. J Hum Hypertens 26, 533–539 (2012). https://doi.org/10.1038/jhh.2011.67
- post-exercise hypotension
- strength exercise
- blood pressure
Science & Sports (2019)
Journal of Clinical Medicine (2019)
Journal of Strength and Conditioning Research (2019)
Postexercise Hypotension After Aquatic Exercise in Older Women With Hypertension: A Randomized Crossover Clinical Trial
American Journal of Hypertension (2018)
Moderate Aerobic Training Decreases Blood Pressure but No Other Cardiovascular Risk Factors in Hypertensive Overweight/Obese Elderly Patients
Gerontology and Geriatric Medicine (2018)