The condition in which a single bout of mild-to-moderate exercise leads to a postexercise decrease in blood pressure (BP) is called postexercise hypotension (PEH). The existing evidence suggests that PEH occurs after aerobic exercise sessions as well as resistance exercise sessions [1, 2]. Recently, a positive association was demonstrated between PEH and long-term effects of exercise training, suggesting that PEH is a predictor of the effects of training on BP [3]. However, the data showing this relationship were mostly based on aerobic training, while resistance training (RT) remains poorly studied [3,4,5]. Moreover, there is a lack of data on this effect in middle-aged hypertensive individuals undergoing treatment, who are usually asymptomatic. Thus, the aim of the present study was to determine whether there is an association between PEH and chronic changes in BP in middle-aged hypertensive individuals undergoing treatment after 8 weeks of RT. PEH was evaluated weekly throughout the follow-up period.

This is an uncontrolled pilot study involving hypertensive individuals enrolled in an RT program. Before and after the exercise intervention (48–72 h after the last exercise session), the subjects underwent body composition and office blood pressure (OBP) evaluations. The subjects completed three exercise sessions a week for 8 weeks, and PEH and OBP were evaluated once a week throughout the 8-week follow-up period. During the intervention, the participants were asked to not alter their diet, to not perform physical exercises other than those recommended for the study and to maintain the same antihypertensive medication.

Patients were recruited from the community. Complete exercise, medical, drug and hypertension histories were recorded. The study inclusion criteria were as follows: (1) individuals using antihypertensive medication; (2) individuals with a BP in the target normal range (120–80 mmHg) or below; and (3) individuals 30–59 years of age. The exclusion criteria were as follows: (1) BMI > 40 kg/m2, (2) participation in regular exercise training within the previous 6 months; (3) a change in antihypertensive drugs within the previous 4 weeks or during the study; and (4) the use of tobacco products. The study was approved by the local ethics committee and was performed in accordance with the current (2013) version of the Helsinki declaration.

Standing height and body weight were measured using standard anthropometric procedures. Muscle thickness measurements were obtained using a LOGIQ-E ultrasound system equipped with a 9.0 MHz linear-array transducer (General Electric Medical Systems, Milwaukee, WI, USA). BP measurements were made using an automated oscillometric device (Omron, HEM-907, Japan) after the patients rested in the sitting position. OBP was accessed once a week before the last exercise session of the week. PEH was accessed in a quiet room after 30 min of rest. To calculate the ∆ PEH, the PEH values were subtracted from the OBP values recorded before the RT session. Associations between ∆ PEH and chronic effects of RT were assessed with respect to the first-week PEH values and changes in OBP (∆ OBP).

The RT protocol consisted of 2–3 sets of 10–20 submaximal repetitions. To prevent the BP from peaking during exercise sessions, individuals performed the target range of repetitions of the following exercises at the maximum weight that they could move with a good technique (without concentric failure): bench press, leg press, lat pulldown, leg extension, shoulder press, leg curl, bicep curl, triceps pulley [6].

The data were analyzed using the statistical package SPSS (Statistical Package for Social Sciences), version 22.0 (IBM, USA). The Shapiro–Wilk test was performed to verify the assumption of normality. Paired t-tests were used to compare the initial values with the postexercise values and the baseline values with the follow-up values. The associations between ∆ PEH and chronic changes in OBP were analyzed by Pearson’s product-moment correlation. The significance level for the α error was set at P < 0.05. The data are presented as the mean ± standard deviation.

Nine middle-aged hypertensive individuals (47.2 ± 6.6 years, 4 males and 5 females) completed the 8-week follow-up. Six individuals dropped out of the study due to personal reasons. Individuals who did not complete the follow-up were excluded. We found a significant effect of time on biceps thickness (p = 0.003) and quadriceps thickness (p = 0.009) after training. There was a significant decrease in systolic OBP over the follow-up period (∆ = −6 ± 4.9 mmHg, p = 0.003) but not in diastolic OBP (∆ = −2.7 ± 4.9 mmHg, p = 0.142). Table 1 shows the data recorded at baseline and at the last follow-up. Table 2 presents the weekly OBP and ∆ PEH measurements. Diastolic PEH did not occur during the intervention. However, significant systolic PEH was observed from the first to the sixth week of the intervention (1°wk: p = 0.012; 2°wk: p = 0.012; 3°wk: p = 0.014; 4°wk: p = 0.014; 5°wk p = 0.014; 6°wk: p = 0.02; 7°wk: p = 0.243; 8°wk: p = 0.312). Finally, we found a moderate positive correlation between the first-week systolic PEH and ∆ systolic OBP (r = 0.675, p = 0.042).

Table 1 General characteristics of the sample
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Table 2 Weekly variations on blood pressure
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The present pilot study shows a moderate association between systolic PEH and ∆ systolic OBP after 8 weeks of supervised RT. However, this association was not found in the diastolic BP measurements. We confirm the results of previous investigations suggested that acute systolic PEH is a predictor of chronic changes in systolic OBP [4, 7, 8]. This is an important finding since no clinical data regarding the predictiveness of PEH in this population have been previously reported. In addition, systolic OBP significantly decreased over the follow-up period (−6 ± 4.9 mmHg), even when the participants used antihypertensive drugs. Therefore, we confirm that our RT program was effective in lowering BP, although BP was well controlled with medications [6].

Another interesting finding was that systolic PEH significantly changed from the first to the sixth week of training; however, a significant difference was not found in the seventh and eighth weeks. The low initial OBP values presented in the last 2 weeks are probably linked with low PEH, since high rest OBP values are related to a higher PEH effect [9]. Thus, the absence of PEH in the last weeks can also be a useful marker on the basis of which the training load/volume can be adjusted to extend the cardiovascular protective effect of PEH. In conclusion, our results provide useful information for individual improvements in BP, exercise prescriptions and the development of training strategies.