We aimed to investigate the effects of endurance training intensity (1) on systolic blood pressure (SBP) and heart rate (HR) at rest before exercise, and during and after a maximal exercise test; and (2) on measures of HR variability at rest before exercise and during recovery from the exercise test, in at least 55-year-old healthy sedentary men and women. A randomized crossover study comprising three 10-week periods was performed. In the first and third period, participants exercised at lower or higher intensity (33% or 66% of HR reserve) in random order, with a sedentary period in between. Training programmes were identical except for intensity, and were performed under supervision thrice for 1 h per week. The results show that in the three conditions, that is, at rest before exercise, during exercise and during recovery, we found endurance training at lower and higher intensity to reduce SBP significantly (P<0.05) and to a similar extent. Further, SBP during recovery was, on average, not lower than at rest before exercise, and chronic endurance training did not affect the response of SBP after an acute bout of exercise. The effect of training on HR at rest, during exercise and recovery was more pronounced (P<0.05) with higher intensity. Finally, endurance training had no significant effect on sympathovagal balance. In conclusion, in participants at higher age, both training programmes exert similar effects on SBP at rest, during exercise and during post-exercise recovery, whereas the effects on HR are more pronounced after higher intensity training.
Studies have shown a direct, strong, independent and continuous relation between blood pressure (BP) and cardiovascular (CV) mortality without any evidence of a threshold down to at least 115/75 mm Hg.1 Further, it has been demonstrated that, as compared with optimal BP, normal and high-normal BP are associated with a higher incidence of CV disease on 10-year follow-up.2 Moreover, a continuous gradient of increasing risk was observed across the three non-hypertensive BP categories.2 Next, a high resting heart rate (HR),3 slow HR recovery after acute exercise 4, 5 and impaired cardiac autonomic function, which is noticeable by decreased HR variability (HRV),6, 7 are all independent predictors of CV disease and mortality across diverse populations.
Physical activity is recommended for the prevention of CV disease in general, and for the prevention, treatment and control of high BP in particular.8, 9 However, increasing rates of urbanization and associated behavioural changes have led to a higher prevalence of a sedentary lifestyle in Western Societies. Moreover, whereas aging is associated with an impairment of autonomic balance and an increase in BP, daily exercise tends to decrease in older participants.10 When recommending physical activity, the dose-response question is an important issue. It refers to the relation between increasing doses of physical activity and changes in a defined health parameter. Nowadays, unanswered questions with practical and clinical implications include will older sedentary individuals reduce their CV risk if they perform exercise at lower intensity (LI) and if so, are these improvements similar to those obtained with an identical training programme at higher intensity (HI)?9 A better understanding of the physical activity dose-response relation is important, particularly in an aging population at increased risk of developing CV or other chronic diseases. If physical activity at LI is effective, it could then be easily recommended to the older sedentary individuals and contribute to a reduction of CV risk at higher age.
A meta-analysis on the influence of aerobic endurance training on BP could not satisfactorily answer the question on training intensity and BP.11 Further, regular physical activity has been shown to lower resting HR;12 to improve HR recovery after acute exercise12, 13 and to increase global HRV14, 15, 16 in several studies, though not all.15, 17, 18, 19 These equivocal results could be because of differences in training characteristics. That is, results from individual studies suggest that indexes of HRV may be more beneficially modulated when training is performed at higher intensities.20 However, most of these studies also differ with regard to study participants, training duration, modalities and frequency. Therefore, there is need for randomized crossover studies in which each participant is trained at both LI and HI, and in which duration, frequency and mode of training are held constant.
The current report was performed, and should be seen, in the context of the overall study protocol of a more comprehensive research trial,21 in which we primarily aimed to investigate whether training at LI (33% of HR reserve (HRR)) has an effect on BP, CV risk factors and BP-regulating mechanisms, and whether the effect is comparable with an identical training programme at HI (66% of HRR) in at least 55-year-old healthy sedentary men and women.
We already performed that both training intensities reduced systolic BP (SBP) at rest and during submaximal exercise by approximately 4–6 mm Hg, whereas only HI training significantly reduced DBP (diastolic BP).21 Hence, the aim of the current report was to investigate whether endurance training at lower intensity has (1) an effect on SBP and HR at rest before exercise, during exercise and after a maximal graded exercise test; and (2) on parameters of HRV, a measure of autonomic nervous system activity at rest before exercise and during recovery from the maximal exercise test in these participants; and (3) whether this effect is comparable with an identical training programme at HI.
Participants and methods
A detailed description of study design, eligibility criteria, screening, training intervention and main results have been published previously.21
Healthy sedentary non-smoking men or women who were at least 55 years old with SBP⩾120 mm Hg or DBP⩾80 mm Hg, and who had no physical limitations that precluded exercise participation were recruited from the general population. Participants were not receiving pharmacological treatment known to affect BP, BP-regulating mechanisms or CV risk factors, and none of the participants had a high or very high CV risk which would require treatment according to prevailing guidelines.8 Approval was obtained from the ethical committee of the Faculty of Medicine of the Catholic University of Leuven. Participants gave a written informed consent.
We used a randomized crossover design comprising three 10-week periods (Figure 1). In the first and third period, participants exercised at LI (33% of HRR) and HI (66% of HRR), respectively, in random order, with a sedentary period in between. Eligible participants were randomized to one of the following sequences: sequence I=LI–sedentary–HI, or sequence II=HI–sedentary–LI. Participants were evaluated at baseline and at the end of each 10-week period. After each training period, evaluation took place on average 3 days (range: 2–7 days) after the last exercise bout.
The training programmes involved supervised sessions with participants exercising (walking/jogging/running (23 min), cycling (23 min) and stepping (5 min)) 3 days per week for 50 min per session at 33% (LI) or 66% (HI) of HRR, excluding warming up and cooling down. Exercise intensity was monitored by Polar HR monitors (Polar Electro, Kempele, Finland) and work rate was automatically adjusted to maintain target HR.
All measurements were performed at the same time of day between 0800 hours and 1300 hours. Participants were asked to have a light breakfast without caffeine. First, they sat quietly in a comfortable chair for 15 min while three suitable electrocardiogram (ECG) leads (ECG monitor 78353A, Hewlett Packard, Boeblingen, Germany) were registered and sampled by a computer for HRV analyses. Then, BP was measured on the left arm, thrice at 2-min intervals by the auscultatory technique using a conventional mercury sphygmomanometer. Next, a 10-min submaximal exercise test at 50% of baseline VO2peak was performed to assess submaximal steady state HR and BP as reported previously.21 Then after 5 min of rest, participants carried out a maximal graded cycle-ergometer test (Ergometrics 8005, Ergometrics, bitz, Germany) with respiratory gas analysis (2900ZR, Sensormedics, Bilthoven, The Netherlands). The initial workload of 20 W was increased by 20 W every minute until volitional fatigue. HR from the ECG and respiratory gas analysis were monitored continuously, and BP was measured at every 2 minutes by the auscultatory technique (STBP-780, Colin, Komaki, Japan). After reaching maximal volitional fatigue, participants cycled for another 8 min at 60 W to avoid syncope. Thereafter, they returned to the chair and a period of 60 min of inactive recovery followed. During this inactive recovery period, HR was monitored continuously from the ECG and BP was measured every 5 min by the auscultatory technique (STBP-780, Colin). Further, starting at minutes 7 and 30 after the start of inactive recovery, the ECG was sampled over a 20-min period for HRV analysis. Owing to the difficulties in measuring DBP with the auscultatory technique during exercise, these results are not reported.
Off-line signal processing was performed to analyze the records. After R-R peak detection and visual inspection by the investigator, a file containing the consecutive R-R intervals was exported. The tachogram of each recording was displayed on a computer screen and a stationary section from the tachogram, free of ectopic beats and artefacts, and as close to the end of each recording as possible, was chosen for further analysis. Analyses were performed on segments of 512 consecutive beats, unless only shorter periods seemed suitable for analysis; a previous study showed that the results from power spectral analysis were similar when periods of 512, 256 or 128 beats were used.22 Premature supraventricular and ventricular beats, missed beats and pauses were filtered and replaced by an interpolated value. Subsequent analysis was performed using methods published previously by Aubert et al.23 Power spectral analysis of HRV was performed by Fast Fourier Transform algorithm. Power spectral analysis allowed estimating the power in the low frequency (LF) and in the high frequency (HF) range. The total power in the frequency range from 0.04 to 0.4 Hz was divided into a LF (0.04–0.15 Hz) and a HF (0.15–0.4 Hz) frequency band.24 Signal powers of each band were calculated as integrals under the respective power spectral density functions. We expressed the LF and HF powers in normalized or relative units, that is, the absolute power divided by the partial power (0.04–0.4 Hz). In addition, the ratio between LF and HF power was calculated. All softwares were developed in house by the Laboratory of Experimental Cardiology using Labview 6.1 (National Instruments, Austin, TX, USA) for Windows.
Data analysis was performed using SAS software version 8.2 (SAS Institute Inc, Cary, NC, USA). Data are reported as mean (standard deviation (s.d.)) or (standard error (s.e.)). SBP and HR during the recovery period were averaged for every 15 min, starting on assumption of the sitting position in the chair (inactive recovery). Variables, which were not normally distributed, were transformed using the natural logarithm (ln) before statistical analysis.
For each training intensity, we first analysed the overall effect of training on SBP and HR at rest and during exercise up to 120 W by using analysis of variance (ANOVA), with phase of training (before and after training), exercise test stage (rest, 40 W, 80 W and 120 W) and participants (nested within its sequence) as sources of variance, and tested the interaction between training and exercise test stage. Next, we analysed whether there was a difference in the response between LI and HI training using ANOVA with treatment (LI or HI), exercise test stage (rest, 40 W, 80 W and 120 W) and participants (nested within its sequence) as sources of variance; baseline values were added as covariates in these analyses.
Similarly, we analysed the overall effect of training on SBP, HR and HRV at rest and in the recovery period for each training programme separately by ANOVA with training phase (before and after training), recovery stage (hence forward called experimental stage (rest, R0–15, R20–30, R35–45, R50–60 for SBP and HR; or rest, R7–27, R30–50 for HRV)) and participants (nested within its sequence) as sources of variance, and we tested whether values at different time intervals into recovery differed from values at rest before exercise by means of a Tukey's post hoc test. Thereafter, we evaluated whether the training effect differed according to the intensity of training using ANOVA with treatment (LI or HI), recovery stage and participants (nested within its sequence) as sources of variance and baselines value as covariates. The Ftr-value refers to the effect of training or the effect of training intensity; the Fl-value refers to the effect of exercise or experimental stage; and the Fi-value refers to the interaction between the stage of activity and the effect of training or intensity. Statistical significance was accepted at P⩽0.05 for two-tailed test.
In the main study, 39 of 48 participants could be included in the final analysis,21 but owing to technical problems during the exercise tests in three participants, only data of 36 participants (17 men) were available for this part of the study: 20 in sequence I and 16 in sequence II. Age at the start of the study for the remaining 36 participants averaged 59 years (range: 55–71 years), weight was 75.7 (s.d. 17.4) kg, and height 1.69 (s.d. 0.089) m. There were no significant differences between baseline values before each training period for any of the variables.
Data at rest and during the maximal exercise test
As shown in Table 1, SBP was lowered by LI (Ftr=10.1; P<0.01) and HI training, (Ftr=15.4; P<0.001) both at rest and during exercise, without significant interaction with the exercise test stage (P>0.50 for all). Comparison of both LI and HI training programmes revealed no significant differences in the response of SBP to training (P=0.35). Further, HR was reduced after LI (Ftr=8.11; P<0.01) and HI (Ftr=29.37; P<0.001) training without significant interaction with the exercise test stage (P⩾0.50). However, the decrease in HR after training was more pronounced after HI compared with LI training (P<0.05).
Data at rest and during recovery after the exercise test
Figure 2 shows SBP at rest before exercise and during the recovery period after the maximal exercise test, both before and after training at LI and HI. Compared with the untrained state, SBP was significantly lower after training at LI (Ftr=18.35; P<0.001) and HI (Ftr=34.16; P<0.001) without interaction with the experimental stage (Fi=0.20 for LI and Fi=0.96 for HI). Further, responses of SBP were similar after LI and HI training (Ftr=1.23, P=0.27). The lack of a significant effect of experimental stage (Fl=0.85 for LI and Fl=0.56 for HI) implies that, SBP during the recovery period did not differ from pre-exercise rest SBP. Results for DBP were roughly similar (data not shown).
The HR at rest and during recovery, before and after training at LI and HI is shown in Figure 3. HR was higher during recovery than before exercise, up to 45 min after exercise. Compared with baseline, both LI (Ftr=29.33; P<0.001) and HI (Ftr=55.14; P<0.001) significantly reduced HR at rest and during recovery without interaction with the experimental test stage (Fi=0.26 for LI and Fi=0.08 for HI). The reduction was more pronounced after HI training than after LI training (Ftr=8.49; P<0.01).
Table 2 shows the results of HRV at rest before exercise and during recovery, before and after training at LI and HI. Total power of HRV was significantly increased after LI training and showed a non-significant trend to increase after training at HI. Both relative powers, that is, LF (%) and HF (%), did not change after training at LI and HI, resulting in an unchanged LF/HF ratio. There were no interactions with the experimental stage for any of the variables. During recovery, the relative HF power remained significantly reduced compared with rest values before exercise, whereas there was no change for relative LF power. As a consequence, LF/HF ratio during the whole recovery period was on an average higher compared with the pre-exercise rest value. Finally, comparison of both training programmes did not reveal differences in the responses of any of these variables.
The main results of the current report show that in the three conditions, that is, at rest, during exercise and during recovery from maximal exercise, both training programmes reduce SBP significantly and to a similar extent. Further, SBP during recovery was, on average, not lower than at rest before exercise, and endurance training did not affect the response of SBP to an acute bout of exercise. Finally, the effect of training on HR at rest, during exercise and recovery was more pronounced with HI training.
As previously reported, a significant increase of VO2peak was observed after training at LI (+10%; P<0.001), which was however more pronounced (P<0.05) after training at HI (+17%; P<0.001).21 The effects of improved fitness on BP, HR and HRV could, therefore, be evaluated in the current report. The present results show comparable reductions of SBP at fixed absolute workloads during the maximal graded exercise test. The decrease averaged 3–8 mm Hg, which is in agreement with previous studies showing a decrease in exercise SBP at fixed absolute workloads.9, 25
An acute bout of exercise elicits a number of transient physiological responses, whereas accumulated bouts of acute exercise produce more permanent chronic adaptations that may be termed the exercise training response.26 Several of the potentially favourable changes in CV risk factors, previously considered to require long-term endurance training, are now known to have both an acute and a chronic exercise component.26 Kraul et al.27 were the first to observe an immediate reduction in BP after a single bout of exercise. This phenomenon may have significant benefits by lowering BP for certain periods of the day. However, given that most of the literature documenting this BP reduction after acute exercise comes from sedentary participants, the possibility remains that this acute effect is merely owing to the effect of a novel stressor on a sedentary system.28 Irrespective of the training programme, on an average, a single bout of exercise did not cause significant reductions in SBP during the 60-minute recovery period compared with pre-exercise rest values in our participants. Whereas significant BP reductions during recovery have been well documented after a single bout of dynamic aerobic exercise in humans with hypertension, its occurrence in normotensive humans is inconsistent.9, 29, 30 Further, if it was observed in normotensive individuals, it was found to be of lesser magnitude than in hypertensives.9, 29, 30 The fact that all our participants, except five, had normal or high normal BP8 corresponding to prehypertension 31 at the start of the exercise test could explain the absence of significant BP reductions during recovery compared with rest values in the overall analysis. Further, we cannot exclude the fact that a short-lasting BP reduction would have occurred if the participants had assumed the sitting position immediately after the maximal exercise test, but to avoid syncope we included an 8-minute active recovery period. We are not aware of any intervention study investigating the effect of chronic endurance training on the effects of a single bout of exercise. We found SBP during recovery to be lower after training compared with the untrained state, but without interaction with the experimental test stage. The latter is in agreement with the cross-sectional data of Senitko et al.,32 who reported no difference in the level of post-exercise hypotension after an acute bout of exercise between endurance-trained athletes and sedentary participants. Further, only recently, Dujic et al.33 showed a reduction in BP after a short maximal field exercise in moderately trained soccer players. However, no control observation or non-athletes were included, hence it is difficult to interpret these results.
The present data further show that both training programmes induced reductions in HR at the same absolute work loads during the maximal graded exercise test, that is, at the loads of 40, 80 and 120 W. Moreover, in agreement with others,34, 35 we found aerobic conditioning to be more pronounced after HI compared with LI training, that is, HI induced a more pronounced reduction in HR and a more pronounced increase in VO2peak during the exercise test compared with LI training. The current results show an elevated HR during the first 45 min of recovery compared with pre-exercise rest values, which is consistent with previous data,36, 37, 38 but in contrast to Perini et al.18
With regard to the spectral components of HRV, we observed that the relative LF component in the recovery period was not different from pre-exercise rest values,37, 38, 39 whereas the HF component during the recovery period was slightly lower than control.37, 38 We have not assessed HRV during exercise, but in an earlier study40 in which we measured HRV during submaximal exercise (up to 40% of maximal workload), we found a slight increase of the relative LF component from 34 to 41%, and a pronounced decrease in the relative HF component from 32 to 9%. The slightly reduced HF component recorded post-exercise in comparison with the pre-exercise stage may indicate that parasympathetic withdrawal contributes to autonomic control of the post-exercise tachycardia.37, 39 However, it is likely that other phenomena played a more important role, such as the higher body temperature and stimulation of circulating catecholamines.41, 42
Cross-sectional data showed that endurance-trained participants exhibit a more rapid HR recovery than their untrained counterparts after exercise at similar relative work loads.43, 44 Concordant to some intervention studies,13, 45, 19 but at variance with others,17, 18 we found HR recovery to be significantly faster after HI training, and to a lesser extent, also after LI training. Training did not affect post-exercise HRV, which is compatible with the observations of Perini et al.,18 Märtinmaki et al.17 and Verheyden et al.,19 who also did not find any change in post-exercise HRV after, respectively, 8 weeks, 14 weeks and 1 year of low to high-intensity endurance training. In addition, there was no difference between LI and HI so that the faster HR recovery with HI is probably not entirely related to differences in the sympathovagal balance, which was in turn not dependent on training intensity. The latter is in agreement with Yamamoto et al. who reported further decreases in HR after the seventh day of training together with unchanged LF/HF ratio.36 Adaptations of intrinsic cardiac rhythm could be a mechanism responsible for this.46 Moreover, the extent to which measurements of HRV and HF reflect parasympathetic tonic activity has still not been clearly established.47 It is thus possible that there exists differences in tonic parasympathetic activity, but that this is not adequately captured by the assessment of HR modulations such as HRV.
Our study has some limitations. It is important to note that the effect of a single bout of exercise on BP was studied after a maximal graded exercise test in the context of the overall study protocol and not in response to a continuous submaximal test, which is usually the case for studies focussing on post-exercise hypotension. Further, because pharmacological treatment was not allowed during the 30-week duration of the study, we excluded participants with high to very high CV risk,8 so that the results may not apply to participants with higher BP levels or participants at higher risk. Another limitation with regard to HRV is that, we did not control respiration and that data were collected in conditions with spontaneous respiration. However Iwasaki et al.48 showed that respiratory rate is not affected by moderate intense exercise training, during four or more sessions per week, for up to 12 months. Therefore, the likelihood that the training programmes in our study would have induced a coherent shift in the respiratory rate, which could have influenced the HRV indexed, is rather low.
In summary, 10 weeks of aerobic endurance training at LI or HI reduces SBP at rest, during maximal exercise and during recovery after the maximal exercise test to a similar extent. In this population of participants with mainly normal or high normal BP post-exercise, SBP was on average not lower than SBP before exercise and chronic exercise training did not affect the effect of a single session of exercise on BP. Finally, in contrast to BP, the effects of training on HR at rest, during exercise and recovery after exercise were more pronounced with HI than with LI.
Conflict of interest
The authors declare no conflict of interest.
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The study was supported by grant G.0562.05 of the Fonds voor Wetenschappelijk Onderzoek—Vlaanderen, Brussels, Belgium.
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