Postexercise Decrease in Arterial Blood Pressure, Total Peripheral

Home , Vascular resistance

Journal of Human Hypertension (1998) 12, 855–860  1998 Stockton Press. All rights reserved 0950-9240/98 $12.00 http://www.stockton-press.co.uk/jhh ORIGINAL ARTICLE Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension

E Izdebska1, I Cybulska2, M Sawicki2, J Izdebski3 and A Trzebski1 1Department of Physiology, Medical University of Warsaw; 2National Institute of Cardiology, 3National Centre of Sports Medicine, Warsaw, Poland

The objective of our study was: (1) to compare the mm Hg, total peripheral resistance (TPR) by 0.45 ؎ 0.05 influence of moderate exercise on circulatory after- TPR u. (33.7 ؎ 2.7%), and in arm vascular resistance response in mildly hypertensive (n = 8) and normoten- (AVR) by 11.0 ؎ 2.7 PRU u. (35.6 ؎ 7%), was observed sive male subjects (n = 9); (2) to examine the circulatory over a 60-min postexercise period. response to 3-min hyperoxic inactivation of arterial NTS exhibited insignificant changes in SBP, DBP, chemoreceptors at rest and during postexercise period AVR except a significant decrease in TPR limited only to in both groups. Hypertensive men (HTS) with a systolic 20-min postexercise period. Hyperoxia decreased SBP, -blood pressure (SBP) 148 ؎ 5 mm Hg, diastolic blood DBP and TPR in HTS. This effect was significantly atten -pressure (DBP) 92.4 ؎ 4 mm Hg; and normotensive men uated during the postexercise period. Long-lasting anti NTS), with a SBP 126 ؎ 3 mm Hg, DBP 75.6 ؎ 1.3 hypertensive effect of a single dynamic exercise in HTS) mm Hg, were submitted to 20-min of moderate exercise suggests that moderate exercise may be applied as an on a cycloergometer (up to the level of 55% of each sub- effective physiological procedure to reduce elevated ject’s resting heart rate reserve). Finger arterial BP was arterial BP in mild hypertension. We suggest also that recorded continuously with Finapres, impedance re- the attenuation of the sympathoexcitatory arterial ography was used for recording stroke volume, cardiac chemoreceptor reflex may contribute to a postexercise output and arm blood flow. In HTS a significant decrease in arterial BP and in TPR in mildly hyperten- .decrease in SBP by 14.5 ؎ 3.4 mm Hg, DBP by 8.9 ؎ 1.9 sive subjects

Keywords: exercise; blood pressure; vascular resistance; arterial chemoreceptor reﬂex; hyperoxia

Introduction temic and regional haemodynamic changes responsible for the postexercise fall in BP. Metabolic vaso- Regular, dynamic, aerobic physical activity is asso- 10 1,2 dilatation, thermoregulatory vasodilatation, ciated with a reduced risk of hypertension A decrease in sympathetic activity,11,13 and resetting of significant inverse relationship between regular the baro- and cardiopulmonary reflex sensi- physical activity and blood pressure (BP) has been 12,14,15 3 tivity have been proposed as possible mech- reported, although some data did not confirm anisms of postexercise hypotension. favourable effects of exercise in essential hyperten- 4,5 One of the possibilities, not yet explored, may be sion. an attenuation of the sensitivity of the sympathoex- In recent years, there has been considerable inter- citatory arterial chemoreceptor reflex (ACR). An aug- est in circulatory after-effects of single physical 6–16 mented responsiveness of ACR in primary hyperten- exercise. Many studies demonstrated that arterial sion has been shown by Trzebski et al18–21 Tafil- BP in hypertensive patients is decreased for hours 20 22 6–8,11,14–16 Klawe et al , and Izdebska et al and is manifested after single dynamic exercise. These stud- by a slight, yet significant, transient fall in arterial ies were done mostly in middle-aged subjects with 6–8,16,17 BP and total peripheral vascular resistance (TPR) in essential hypertension. young mildly hypertensive subjects exposed to brief There are inconsistencies with regard to the sys- hyperoxia, a condition which inactivates the neuro- genic sympathoexcitatory reflex drive from the peripheral arterial chemoreceptors and reduces sym- Correspondence: Dr Ewa Izdebska, Department of Physiology, 23 Medical University of Warsaw, Krakowskie Przedmiesćie 26/28 pathetic nerve activity at rest. str,. 00–927 Warsaw, Poland No systematic study has been done on the haemo- Received 24 January 1998; revised 14 July 1998; accepted 13 dynamic effects of inactivation of the arterial August 1998 chemoreceptors in hypertensive human subjects Postexercise hypotension, hyperoxia, essential hypertension E Izdebska et al 856 during postexercise period. The problem appears of about 55% of each subject’s resting heart rate interesting, as regular physical exercise has been fre- reserve, which corresponded to the external power quently recommended for the prevention and output of 116 ± 4 and 119 ± 4 Watts for HTS and attenuation of arterial hypertension. NTS, respectively. Therefore the aim of our study was: A short-lasting inactivation of the arterial chemoreceptors was produced by a brief breathing from a (1) To test the influence of moderate exercise on the mixture of 60–70% oxygen in air from a 200 litre cardiovascular system in young mildly hyper- Douglas bag for a 3-min period. The measurements tensive subjects and in a matched normotens- were performed: during the 60-min rest period ive group. (control), during the 20-min dynamic exercise, and (2) To examine the circulatory response to the hyp- during the 60 to 90-min recovery. In the same sub- eroxic inactivation of arterial chemoreceptors at jects periods of brief hyperoxia were applied 10 min rest and during postexercise period. before and 50 min after the cessation of exercise, when the BP was stable. Subjects and methods All measurements were performed in the standardised condition. Each subject was in the sitting This study was approved by the National Institute position on the cycloergometer over all experi- of Cardiology ethics’ committee on human research. mental periods, with both hands fixed in the hori- Each subject gave written consent to participate in zontal plane at the level of the tricuspid valve. Such the study. conditions enabled us to maintain stable and repro- Measurements were performed on eight untreated ducible measurements. mildly essential hypertensive (HTS, aged 26 ± 4 For the statistical analysis, repeated measure- years) and nine healthy normotensive male subjects ments ANOVA and Dunnett’s test were used for esti- (NTS, aged 25 ± 3 years). All subjects were found to mation of the differences between control pre-exer- be free from pulmonary, renal and heart diseases. cise value and postexercise values of systolic BP Characteristics of both groups are presented in (SBP), diastolic BP (DBP), CO, TPR in the same Table 1. group of NTS and HTS independently. One-way Finger arterial BP was measured continuously analysis of variance was used to compare mean post- with Finapres (Ohmeda). A tetrapolar impedance exercise values of HTS and NTS groups. Student’s reography (Warsaw Technical University) was used t-test was used for the estimation of statistical sig- to compute continuously stroke volume, cardiac nificance of differences between control values of output (CO) and arm muscular blood flow (ABF). both groups and each mean of respective before and The first derivative of the impedance change after hyperoxia means (unpaired and paired t-test, (associated with ventricular contraction) was used respectively). Correlations were calculated by linear to calculate stroke volume, using the Kubicek equ- regression. Values were considered significant if ation.24–26 TPR was calculated in TPR units by divid- they achieved a P value р0.05. Results were ing mean arterial BP by cardiac output. Arm regional expressed as mean ± standard error of mean (s.e.m.). vascular resistance (AVR) was calculated per 100 ml tissue/min in PRU units. Heart rate (HR) was measured from the ECG recordings. All data were Results synchronously sampled on five channels and col- lected continuously on-line with a sampling fre- Effects of exercise quency of 200 Hz and 12-bite resolution. The data In HTS the exercise caused a significant rise in SBP were analysed with use of the specialised macro lan- from 148 ± 5 mm Hg to 198.5 ± 15 mm Hg, in HR guage adapted to the experimental program. from 73.5 ± 3 to 132.6 ± 2.5 beats/min, in CO from Exercise of an increasing intensity was performed 5.12 ± 0.75 to 13.8 ± 1.45 l/min. TPR decreased sig- on a bicycle ergometer Monark 818E, up to the level nificantly from 1.429 ± 0.24 to 0.648 ± 0.1 TPR u., DBP changed insignificantly from 92.4 ± 4 to 100.2 ± 8.3 mm Hg. Table 1 Resting characteristics of the study population In NTS the same level of exercise caused a sig- ± ± Variable Hypertensive Normotensive nificant increase: in SBP from 126 3 to 201 9.2 mm Hg, in DBP from 75.6 ± 1.3 to 99.7 ± 2.9 mm Hg, ± ± Age (yr) 26 ± 425± 3NS in HR from 73.6 3.7 to 137.3 1.3 beats/min, CO Weight (kg) 92.2 ± 487± 3.5 NS from 6.3 ± 0.57 to 15.1 ± 1.7 1/min and a significant Height (cm) 180.4 ± 1.7 183.4 ± 2NS decrease in TPR from 0.868 ± 0.07 to 0.465 ± 0.05 Resting SBP (mm Hg) 148 ± 5 126 ± 3** TPR u. Resting DBP (mm Hg) 92.4 ± 4 75.6 ± 1.3** HR (beats/min) 73.5 ± 3 73.6 ± 3.7 NS The exercise induced similar increases in heart CO (l/min) 5.12 ± 0.75 6.3 ± 0.57 NS rate in both groups. The external power outputs dur- CI (l/min/m2) 2.4224 ± 0.8 3.078 ± 0.3 NS ing exercise were not significantly different in HTS TPR (TPR u.) 1.429 ± 0.24 0.868 ± 0.07* and NTS subjects (see methods). ± ± AVR (PRU u.) 33 1.9 10 2.63** The mean systolic and diastolic pressure during exercise did not differ between HTS and NTS. The CI = cardiac index, TPR u. = total peripheral vascular resistance units, PRU u. = peripheral regional vascular resistance units, absolute and percentage increase in the systolic and other abbreviations—see text. diastolic BP in NTS (an increase in SBP by 82.8 ± 8 *P Ͻ 0.05, **P Ͻ 0.01. mm Hg; by 65.58 ± 6.3% of control resting value, Postexercise hypotension, hyperoxia, essential hypertension E Izdebska et al 857 and in DBP by 23 ± 3 mm Hg; 20.2 ± 3%) were 13 ± 3.5%, P = 0.01. In contrast, in NTS, CO was greater than those in HTS (an increase in SBP by higher by 13.7 ± 4.8%, P Ͻ 0.01 only over a 20-min 48.2 ± 12 mm Hg; 32.3 ± 7.5% of the control value, postexercise period. and in DBP by 9.46 ± 4.7 mm Hg; 9.9 ± 4.65%, TPR in HTS was significantly lower over the P Ͻ 0.05). whole 60-min postexercise period and even after- During physical exercise TPR decrease in HTS wards. At the end of a 1 h postexercise rest TPR was was significantly greater than in NTS (by 0.845 ± still lower by 27.8 ± 4.8%, P Ͻ 0.01 (Figure 1). In 0.19 and 0.426 ± 0.04, respectively, P Ͻ 0.05). NTS TPR was significantly reduced only over the 20 min postexercise period compared to the control ± Ͻ Arterial BP, cardiac output, total peripheral values by 18.4 2.7%, P 0.01. resistance and arm vascular resistance in the HR was significantly higher in the postexercise postexercise period period in both groups. Over the last 10 min of a 1 h postexercise period it was higher by 7 ± 1.8 SBP and DBP in HTS were significantly lower at beats/min in the HTS, and by 5 ± 0.7 beats/min in 15 min of the postexercise period compared to the the NTS. The difference was not significant. pre-exercise control: by 13.6 ± 3.6 mm Hg and 8.7 ± Ͻ In HTS AVR in the postexercise period was 2.3 mm Hg, P 0.05, respectively. After 60 min reduced by 35.6 ± 7%, P Ͻ 0.05. In NTS AVR was since the end of exercise these values have been still reduced over a 25-min postexercise period by 13 ± reduced by 16.5 ± 3.6 mm Hg and 8.9 ± 1.9 mmHg, 4.6%, abating thereafter (Figure 2). respectively, P Ͻ 0.01 (Figure 1). The absolute values of SBP, DBP and TPR during In contrast, in NTS only nonsignificant decrease in SBP and DBP were observed by 2 ± 2.8 and 3.4 ± the postexercise period did not significantly differ 2.5 mm Hg, respectively during postexercise period between both groups, despite significantly higher (Figure 1). respective values in the hypertensive group in the CO in HTS was significantly higher during the control rest period. postexercise recovery period compared to the pre- In HTS a significant positive correlation was exercise control values (Figure 1), and remained observed between the resting DBP values and post- = Ͻ augmented still 60 min after the end of exercise by exercise TPR values, r 0.9937, P 0.001.

Figure 1 (A) Time course of postexercise mean values of the systolic blood pressure (SBP), diastolic blood pressure (DBP) in hypertensive subjects (HTS), and normotensive subjects (NTS). (B) Time course of postexercise mean values of the cardiac output (CO) in hypertensive subjects and normotensive subjects. (C) Time course of postexercise mean values of the total peripheral resistance (TPR) in hypertensive subjects and normotensive subjects. Measurements were taken in pre-exercise control period (time 0), and in every 10 min of postexercise period. Asterisks denote significant difference between mean control pre-exercise values and means calculated for each 10-min period during postexercise period. 0 time = mean value for pre-exercise control period; ! = P р 0.05, !! = P р 0.01; significantly different from HTS; *P р 0.05, **P р 0.01, significantly different from control, pre-exercise value, (time 0). Postexercise hypotension, hyperoxia, essential hypertension E Izdebska et al 858 nificant increase in CO by 12.8 ± 3.6%, P Ͻ 0.05, and a decrease in AVR by 11.5 ± 1.6%, P Ͻ 0.01. HR decreased by 2.6 ± 0.8 beats/min, P Ͻ 0.05. In contrast, in NTS a small yet significant increase in DBP by 1.76 ± 0.64 mm Hg, P Ͻ 0.05, in TPR by 8.9 ± 2.9%, P Ͻ 0.01, and a nonsignificant increase in SBP by 1.15 ± 1.56, were observed (Figures 3 and 4). CO decreased by 5.3 ± 2.1%, P Ͻ 0.05, AVR increased slightly by 5 ± 3%, P Ͼ 0.05, HR decreased by 5.7 ± 1 beats/min, P Ͻ 0.01. Hyperoxia applied during the postexercise period did not significantly change haemodynamic parameters in either group (Figures 3 and 4), except for some decrease in HR in HTS by 3.7 ± 0.38 beats/min, P Ͻ 0.01, and in NTS by 5.3 ± 1.4 beats/min, P = 0.01. However the difference between both groups Figure 2 Mean data for postexercise AVR, during the period start- in HR reduction induced by hyperoxia was non- ing 25 min after the exercise. Other descriptions as in Figure 1. significant. A significant positive correlation between the resting DBP and the decrease in TPR during hyperoxic inactivation of the arterial chemoreceptor reflex was found in HTS subjects: r = 0.9639, P Ͻ 0.01.

Discussion The major finding of our study is a prolonged reduction of the systolic and diastolic BPs during the postexercise period following a 20-min moderate exercise period. Attenuated haemodynamic response to hyperoxia applied 50 min after the end of exercise in the HTS suggests a long-term decreased drive from the arterial chemoreceptors in the postexercise period. Haemodynamic response to exercise itself in Figure 3 SBP and DBP response to short time lasting inactivation hypertensive patients observed in our study is not = of arterial chemoreceptors by brief hyperoxia. CON control rest dissimilar to other reports.6,8,17,22,27,28 period, OX = hyperoxia, CONR = control for recovery period. Other descriptions as in Figure 1. The reduction in BP in the postexercise period was parallel to the increase in CO and decrease in Effects of hyperoxia the total peripheral and arm regional vascular resistance. NTS did not demonstrate significant after- In HTS a short time breathing with oxygen during effects of exercise. Decrease in SBP and DBP was the control pre-exercise period caused a slight yet nonsignificant and increase in CO, decreases in TPR ± significant decrease in DBP by 4.6 0.86 mm Hg, and AVR were of shorter duration in NTS than in Ͻ ± Ͻ P 0.01; in SBP by 9 1.8 mm Hg, P 0.01 (Figure the HTS group. ± Ͻ 3), in TPR by 18.6 1.6%, P 0.05 (Figure 4), a sig- Arterial BP, CO and AVR were measured continuously, non-invasively, in standardised conditions (see methods). No increase in BP before the start of exercise was observed. Therefore, the changes in BP do not appear to be related to a pre-exercise cardiovascular anticipatory reaction. We applied the exercise of moderate intensity because such level of exercise is easily tolerated and is recommended in most training and recreational programmes.29,30 Our results are in agreement with those of Cleroux J et al.6 However our subjects were of younger age, the exercise period was shorter, and we observed more pronounced postexercise decrease in TPR in HTS as compared to the NTS. The haemodynamic pattern during the postexercise period may depend on the age, on the haemodynamic state of the population studied, and on the Figure 4 TPR response to short time lasting inactivation of protocol used. In elderly hypertensive subjects, an arterial chemoreceptors by brief hyperoxia. Other abbreviations increase in TPR, a decrease in cardiac output, no as in Figure 3. Other descriptions as in Figure 1. decrease in DBP, and an unchanged heart rate after Postexercise hypotension, hyperoxia, essential hypertension E Izdebska et al 859 three 15-min bouts of treadmill exercise at 50% VO2 hyperoxia reduces arterial BP whereas in healthy max, were reported.17 No change in DBP was subjects hyperoxia leads to transient increase in TPR observed in borderline hypertensive men during and in arterial BP. postexercise period.11 To summarise: In other studies arterial BP was measured at selec- (1) In mildly hypertensive subjects moderate exer- ted time points by a traditional arm cuff method. In contrast we applied a continuously non-invasive BP cise induces a decrease in arterial BP and total recording beat by beat along with CO, HR and AVR. peripheral resistance and arm vascular resistance. Measurements performed only at selected time points may over- or underestimate fluctuating car- (2) In matched normotensive subjects similar mod- diovascular variables. erate exercise produces only insignificant decrease in arterial BP and total peripheral Physiological mechanisms which account for postexercise hypotension are still unclear.9,30 resistance. Recently, it has been proposed that inhibition of (3) During postexercise recovery period arterial BP and total peripheral resistance values in the sympathetic nerve activity and vasodilatation is responsible for the decrease in arterial BP and in hypertensive subjects are reduced to the values which do not differ from the values in the norm- total peripheral resistance during the postexercise otensive group. period.11,13 An activation of the central opioid endorphin systems by exercise has been suggested (4) A fall in arterial BP and total peripheral resistance produced by short-lasting hyperoxic inacti- to be involved in the postexercise vasodilatation. vation of peripheral arterial chemoreceptors in Such activation decreases sympathetic vasoconstric- tor activity.31 Naloxon, an opioid antagonist, hypertensive subjects is attenuated during postexercise recovery. blocked or attenuated the postexercise hypotension.31,32 A decrease in transmission of the sympathetic activity into blood vessels has also been Conclusions observed after dynamic exercise.13 A reduced vascular alpha-adrenergic responsiveness after acute exer- (1) An attenuation of the chemoreceptor reflex drive cise has been reported in Dahl-salt sensitive rats.33 following moderate exercise may contribute to the The sympathoexcitatory peripheral arterial mechanisms of the reduction of BP and total periph- chemoreceptor reflex is hyperactive in mild arterial eral resistance during the postexercise period in hypertension.18–22,34–36 Our study indicates an mildly hypertensive subjects. attenuation of circulatory BP and TPR response to (2) The present results suggest that moderate exer- brief hyperoxia during postexercise period in hyper- cise may be applied as an effective physiological tensive subjects. This result suggests that augmented procedure to reduce elevated arterial BP in mildly sympathoexcitatory tonic drive induced by over- hypertensive subjects. active chemoreceptor reflex in hypertensive subjects is reduced in the postexercise period. Such a postex- Acknowledgements ercise attenuation of chemoreceptor sympathoexcitatory drive may contribute to reduced sympathetic This project was supported by a research grant from nerve activity observed after dynamic exercise.11,13 the Medical University of Warsaw and KBN Grant Unknown is the mechanism of chemoreceptor No. 4505A 059 09. inhibition in a postexercise period. Inhibitory influences on the afferent activity of arterial chemo- reflex may appear after exercise. Possible candidates References are: nitric oxide (NO), and/or endogenous opioids, 1 Horan MJ, Lenfant C. Epidemiology of blood pressure an inhibitory substance to the glomic chemosensory and predictors of hypertension. 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