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Influence of Recovery Posture on Blood Pressure and Heart Rate After Resistance Exercises in Normotensive Subjects

de Tarso Veras Farinatti, Paulo1,2; Nakamura, Fabio Yuzo3; Polito, Marcos Doederlein3

Journal of Strength and Conditioning Research: December 2009 - Volume 23 - Issue 9 - p 2487-2492
doi: 10.1519/JSC.0b013e3181b25e48
Original Research

Farinatti, PAV, Nakamura, FY, and Polito, MD. Influence of recovery posture on blood pressure and heart rate after resistance exercises in normotensive subjects. J Strength Cond Res 23(9): 2487-2492, 2009-This study investigated the effects of body posture on systolic (SBP) and diastolic (DBP) blood pressure, mean arterial pressure (MAP), and heart rate (HR) after a session of resistance exercises. Twelve normotensive men were randomly assigned to either a control group (CG) or exercise group (EG). The EG performed 4 sets of 10 lifts at 80% of repetition maximum (10RM) using 4 different exercises. The BP and HR were assessed on different days in seated and supine postures at rest and at 10-minute intervals during 30 minutes of postexercise recovery. Except for DBP, a 3-way ANOVA revealed that postexercise SBP in EG was always lower than at rest during seated (minimum of 109.5 ± 1.4 mm Hg at 10 min vs. 119.2 ± 3.4 mm Hg at rest; p < 0.01) and supine recovery (minimum of 112.7 ± 3.0 mm Hg at 20 min vs. 118.4 ± 1.7 mm Hg at rest; p < 0.05). The MAP during recovery in the seated posture was lower than at rest (minimum 83.3 ± 2.6 mm Hg at 30 min vs. 89.3 ± 0.9 mm Hg at rest; p < 0.05), whereas in the supine posture, no difference was identified (minimum 83.6 ± 1.9 mm Hg at 10 min vs. 87.1 ± 1.8 mm Hg at rest; p > 0.05). The HR at 10 minutes (82.0 ± 4.8 bpm; p < 0.01), 20 minutes ([83.7 ± 6.3 bpm; p < 0.05), and 30 minutes (80.5 ± 6.2 bpm; p < 0.01) of recovery during the seated posture was higher than at rest (71.5 ± 2.1 bpm). In contrast, in the supine posture, HR was higher than at rest (66.8 ± 3.7 bpm; p < 0.01) throughout 10 minutes (79.7 ± 5.3 bpm) and 20 minutes of recovery (74.5 ± 4.2 bpm). In conclusion, the postexercise hypotensive response can be affected by posture during BP assessment.

1Laboratório de Atividade Física e Promoção da Saúde (LABSAU), Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil; 2Physical Activity Sciences Post-Graduation Program, Universidade Salgado de Oliveira, Brazil; and 3Department of Physical Education, State University of Londrina, Parana, Brazil

Address correspondence to Paulo Farinatti, or

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Physical exercise is a relevant nonpharmacologic option for the prevention and treatment of blood pressure (BP) disorders. Previous studies have demonstrated that performing a single exercise session can promote a decline in the BP postexercise compared with pre-exercise (6,7,19,33). Such BP decline (postexercise hypotension [PEH]) is an important physiologic phenomenon with clinical implications as a complementary strategy for controlling BP in hypertensive subjects (11).

The PEH occurs frequently after aerobic exercise at intensities higher than 50% of the maximal oxygen uptake (O2max) (19) and probably after exercising at least 10 minutes (20). Although the amount of information available is lower than for aerobic exercise, there have been previous studies suggesting that resistance exercise can also induce PEH when performed at different intensities (28) or session sets (33) in both normotensive and hypertensive subjects (6,22,30).

Several physiologic mechanisms can be associated with PEH. For instance, in young adults, it may be related to a reduction of vascular resistance (3,25) by means of higher endothelium-dependent vasodilatation (8), whereas, in the elderly, a decline in the cardiac output appears to be a determinant factor (10,31).

The PEH mechanisms postexercise can also influence BP response (29), depending on body posture. Therefore, the postexercise BP depends on the body posture during assessment, which may lead to biased data and misinterpretation of results.

Most PEH studies have used seated recovery for BP assessment after aerobic (5,21) or resistance exercises (21,28,33). However, there is evidence to suggest that, in comparison with supine recovery, this posture can interfere with the responses of stroke volume, cardiac output, peripheral resistance, and diastolic BP (DBP) (29). Consequently, it is possible that the assessment posture can introduce bias into the PEH analysis. Despite such a possibility, there is a lack of data to confirm this influence, especially after resistance training. In fact, we could not find studies that had measured the effects of posture on BP after a resistance exercise session.

Therefore, the purpose of this study was to compare the responses of systolic blood pressure (SBP), DBP, mean arterial pressure (MAP), pulse pressure (PP), and heart rate (HR) measured during seated and supine recovery after a session of resistance exercises.

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Experimental Approach to the Problem

The necessary sample size was calculated considering 0.72 mm Hg for the SBP in the last measure as the minimum difference from rest values and 0.34 mm Hg as the residual SD. A statistical power of 80% was predefined for a significance level of p < 0.05 (Primer of Biostatistics 4.0, USA). The results indicate a minimum of 5 subjects are required for each group (experimental [EG] and control [CG] groups). Thus, 12 men participated in the study and were randomly assigned to either the CG (n = 6) or EG (n = 6).

Data were assessed on 4 nonconsecutive days, with 48 hours separating the sessions. During the first 2 days, the 10 repetition maximum (10RM) workload was determined. During the remaining days, the exercise protocols were performed to assess the BP and HR at rest and after the resistance exercises in the different body postures. Therefore, the BP was assessed at rest in the seated and supine postures. The EG performed a resistance exercise session, whereas the CG remained seated. In both groups, the BP was measured for 30 minutes after the end of the session during seated and supine recovery.

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The following exclusion criteria were used to select the subjects: a) diagnosed cardiovascular disease; b) use of drugs that could affect the cardiovascular responses; c) bone, joint, or muscle problems diagnosed that could limit the execution of the exercises. Thus, 12 normotensive men with at least 2 years of recreational resistance training experience were randomly assigned to either a CG (n = 6; height = 1.8 ± 0.1 m; weight = 80.0 ± 4.4 kg; age = 27 ± 1 yr) or EG (n = 6; height = 1.8 ± 0.1 m; weight = 77.4 ± 3.8 kg; age = 27 ± 1 yr) during Spring of 2005. This study was approved by the institutional ethical committee and was conducted according to the Declaration of Helsinki. Subjects were informed about the procedures and risks before giving written consent.

For 12 hours before the experimental day, subjects were required to avoid ingestion of alcohol and caffeine and smoking. In addition, subjects were asked to refrain from physical activity and to be well rested. They were also requested to have their last light meal 3 hours before data assessment, which always took place in the morning, between 9 and 10 am. The ambient temperature was fixed at 20°C to 25°C, and the air humidity during the tests ranged between 60% and 70%.

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Experimental Procedures

The mass of all weight plates and bars used for measuring 10RM was determined with a precision scale. Subjects performed 4 experimental sessions on 4 different days, separated by 2 days of rest. On the first day, 10RM workloads were determined for EG with the following exercises: peck deck, knee extension, chest press, and leg press (Buick, Rio de Janeiro, Brazil). The subjects performed a maximum of 4 attempts to attain 10RM workload of each exercise with 5-minute rest intervals between them. On the second day, the 10RM tests were repeated to establish their reliability (peck deck intraclass correlation coefficient [ICC] = 0.91, p < 0.01; knee extension ICC = 0.89, p < 0.01; chest press ICC = 0.94, p < 0.01; leg press ICC = 0.86, p < 0.01). On these 2 days, the CG did not participate in the measurements.

On the third and the fourth days, subjects performed resistance exercises, and the order of body posture (seated or supine) was randomly assigned. When subjects arrived at the laboratory, they were required to rest for 10 minutes before assessment of resting parameters in either seated (SeEG or SeCG) or supine recovery postures (SuEG or SuCG). Afterward, the EG performed 4 sets of 10 lifts at 80% of 10RM with 2-minute intervals between sets and exercises. While the EG completed the session, the CG remained seated on chairs. After resistance exercises, both groups returned to their initial postures for BP assessment for each 10-minute period during the 30-minute recovery period. The SBP and DBP were measured following the recommendations from the American Heart Association (26) by semi-automatic device (HEM-431 CINT Omron, Vernon Hills, IL, USA), with HR assessed by cardiotachometer (Polar A1, Kempele, Finland). The MAP was calculated by the equation MAP = DBP + [(SBP - DBP) ÷ 3]. The PP was estimated by subtracting DBP from SBP (PP = SBP - DBP).

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Statistical Analyses

The Shapiro-Wilk test was used to determine data normality, and the homogeneity of variances of the whole sample was checked by the Levene test. The results for CG and EG in the different instants were compared by a three-way ANOVA for repeated measures followed by the Fisher post hoc test. In all cases, the significance level was fixed at p ≤ 0.05. The statistical calculations were made using the software Statistica 6.0 (Statsoft, Tulsa, OK, USA).

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There were no statistical differences between the body postures in the postexercise values of SBP (p = 0.59), DBP (p = 0.45), MAP (p = 0.72), PP (p = 0.60), and HR (p = 0.67). The comparisons within the groups (SeEG vs. SuEG and SeCG vs. SuCG) revealed that body posture did not influence cardiovascular responses. Table 1 shows SBP and DBP for EG and CG in each body posture. In SeEG and SuEG, there was a significant decline of SBP in all measurements, but not of DBP. The comparison between SeEG and SuEG did not attain statistical significance for differences in SBP or DBP. The MAP was statistically higher at rest than at all assessments during the seated but not the supine posture (Table 2). On the other hand, PP was statistically lower than at rest only for SuEG at the 30-minute assessment (Table 2).

Table 1

Table 1

Table 2

Table 2

Postexercise HR was always higher than at rest in SeEG. However, in SuEG, the HR at rest was lower than at 10 and 20 minutes after the resistance exercises. Also, the HR at 30 minutes was lower than at 10 minutes (Table 3).

Table 3

Table 3

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The present study investigated the influence of body posture on BP and HR responses to a session of resistance exercises. The results revealed that MAP was lower at rest over 30 minutes after the exercises only in the supine position. In this sense, the major finding of the present study is that the postexercise hypotensive response is affected by posture during BP assessment.

Although few studies have investigated the effects of resistance exercise on BP, there is evidence to suggest that moderate resistance exercise can be part of a nonpharmacologic intervention strategy to prevent and treat high BP (4). However, the PEH clinical significance relies on its duration and magnitude (11), which would enhance the possibility of subacute inhibitory response, leading to a temporal summation able to induce actual adaptations (21).

Studies have reported significant decline in BP after acute resistance exercise applied at different combinations of volume and intensity. These studies reported PEH using seated recovery to assess the BP (1,21,22,28,30,33). However, the cardiovascular responses may be affected by the body posture. For instance, Raine et al. (29) showed that SBP, DBP, MAP, and PP measured in the seated posture did not differ from the supine posture for 30 minutes after a graded, upright cycling protocol to volitional exhaustion, whereas the HR was significantly lower in the latter. Takahashi et al. (34) confirmed these results, showing that, after 15 minutes in a given rest condition, the HR was higher in the seated (81.7 ± 8.6 bpm) than in the supine recovery posture (62.3 ± 6.9 bpm).

In the present study, there were no changes in BP variables in the rest condition. On the other hand, the HR in SuEG was lower (66.8 ± 3.7 bpm), but not significantly, than in SeEG (71.5 ± 2.1 bpm). It is worth mentioning that, in the present study, the subjects remained at rest for 10 minutes before the exercise protocol, whereas Raine et al. (29) asked subjects to rest for 30 minutes. This difference can partially explain the fact that the HR did not decline significantly in SuEG, which would occur if this posture were sustained longer before exercising. However, the SuCG and SeCG values were similar, suggesting body posture does not influence HR response, at least during the investigated term.

One possible explanation for the influence of the body posture upon resting HR relates to blood transfer to the veins, especially in the regions that are below heart level. When the subject is seated or standing, the hydrostatic pressure gradient increases the BP in regions distant from the heart (35). This gravity effect leads to a greater amount of blood shifting into the veins. Because the potential of the muscle pump to stimulate venous return is lower at rest, the cardiac output tends to decrease. Thus, the HR increases to compensate for a lower stroke volume (11), whereas the supine posture tends to transfer blood to the upper body. The enhanced blood and fluid volume centralization increase venous return, which stimulates baroreceptors, increases cardiac filling and stroke volume, and reduces HR reflexively (29).

After exercise, regardless of body posture, the HR values were higher than at rest, even when there was PEH. The mechanism that explains this effect is partially the same as that previously described. In fact, one of the possible causes of PEH is a reduction of peripheral resistance, which can increase blood flow. This enhanced systemic blood flow relates to a higher shunting of blood to the veins, but the venous return decreases because of the absence of muscle contraction. Consequently, the left ventricular end-diastolic volume and the stroke volume decrease, whereas the HR increases to preserve cardiac output (12-14). This HR increase is mediated by cardiac sympathetic activity combined with reduced parasympathetic modulation of sinoatrial nodes (15,30).

Previous studies reported an increase of HR after aerobic (5,17) and resistance exercises (21). Those who assessed HR during supine recovery reported comparatively lower values than those assessing HR during the seated posture (29,34). In the present study, the postexercise HR values of the EG were always higher than at rest, and no difference was detected between the body postures. Nevertheless, in SeEG, the HR remained high for 30 minutes, whereas, in SuEG, it was prevalent only at the first 2 assessments, returning to the resting values at the last assessment. In other words, although no significant difference in HR can be assigned to the effect of body posture, a longer postexercise increase is likely to occur in the seated compared with the supine recovery.

Body posture may influence the postexercise BP responses, but research on this matter is controversial. Raine et al. (29) did not find differences between SBP and MAP as assessed during seated and supine recovery after incremental cardiopulmonary exercise testing protocols of approximately 16 minutes. On the other hand, Raine et al. (29) showed that DBP had larger decreases when measured during supine recovery. Takahashi et al. (34) suggested different conclusions when comparing the cardiovascular responses after 5-minute cycle ergometer exercise at 80% of maximal oxygen uptake. There were no differences between SBP and DBP assessed during 10 minutes in the seated and supine recovery, which may be partially explained by the short period of observation.

In the present study, the SBP decrease in SeEG after the resistance exercises was not statistically different from SuEG. However, the absolute values recorded for SeEG were systematic lower, which suggests that BP responses were more sensitive in this body posture. These data support those reported by Raine et al. (29) because the PEH in SBP was slightly higher at seated (11 ± 3 mm Hg) than at supine recovery (8 ± 3 mm Hg). Such SBP response may influence the MAP postexercise values because MAP was significantly lower than at rest for SeEG, but not for SuEG. An effect of the exercise on the baroreflex control (24) and the gravitational stress during the seated recovery (29,32), potentially enhancing the PEH, could explain these findings. It should be noted that prolonged sitting (i.e., without prior exercise) imposes a great orthostatic stress in men, with consequent hemodynamic changes that raise peripheral resistance and MAP (9). This might help to explain why resistance exercises influenced the SeEG response more than the SuEG.

In conclusion, body posture can influence BP after resistance exercises. The present findings suggest that the seated posture was related to a higher hypotensive response compared with the supine posture. Such results should be taken into account in studies that aim to observe the cardiovascular responses after resistance training sessions.

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Practical Applications

A better understanding of the postexercise cardiovascular responses can be important for some population groups, including those with hypertension or coronary heart disease, as well as among healthy, young subjects, to control long-term resting BP. In this context, the control of body posture during assessment of postexercise cardiovascular responses can be useful for determining the specific influence of resistance exercises on variables such as HR and BP while avoiding misinterpretation bias. The results of the present study indicate that seated recovery is suitable for PEH assessment after resistance exercise because MAP reduction was significant only in this posture, implying that supine recovery may mask the hypotensive response because of reduced orthostatic stress.

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